Cardiovascular diseases (CVDs), including hypertension, atherosclerosis, and cardiomyopathy among others, remain the leading cause of global morbidity and mortality. Despite advances in treatment, the complex pathophysiology of CVDs necessitates innovative approaches to improve patient outcomes. Recent research has uncovered a dynamic interplay between mitochondria and gut microbiota, fundamentally altering our understanding of cardiovascular health. However, while existing studies have primarily focused on individual components of this axis, this review examines the bidirectional communication between these biological systems and their collective impact on cardiovascular health. Mitochondria, serving as cellular powerhouses, are crucial for maintaining cardiovascular homeostasis through oxidative phosphorylation (OXPHOS), calcium regulation, and redox balance. Simultaneously, the gut microbiota influences cardiovascular function through metabolite production, barrier integrity maintenance, and immune system modulation. The mitochondria-gut microbiota axis operates through various molecular mechanisms, including microbial metabolites such as trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFA), and secondary bile acids, which directly influence mitochondrial function. Conversely, mitochondrial stress signals and damage-associated molecular patterns (DAMPs) affect gut microbial communities and barrier function. Key signalling pathways, including AMP-activated protein kinase (AMPK), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and the silent information regulator 1-peroxisome proliferator-activated receptor gamma coactivator 1-alpha (SIRT1-PGC-1α) axis, integrate these interactions, highlighting their role in CVD pathogenesis. Understanding these interactions has revealed promising therapeutic targets, suggesting new therapies aimed at both mitochondrial function and gut microbiota composition. Thus, this review provides a comprehensive framework for leveraging the mitochondria-gut microbiota axis in providing newer therapeutics for CVDs by targeting the AMPK/SIRT-1/PGC-1α/NF-κB signalling.

Cardiovascular disease is one of the leading causes of death worldwide. Even while receiving adequate pharmacological treatment for their hypertension, people are nonetheless at greater risk for cardiovascular disease. There is growing evidence that the gut microbiota may have major positive and negative effects on blood pressure and illnesses related with it as more study into this topic is conducted. Trimethylamine n-oxide (TMAO) and short-chain fatty acids (SCFA) are two major by-products of the gut microbiota. TMAO is involved in the formation of other coronary artery diseases, including atherosclerosis and hypertension, while SCFAs play an important role in controlling blood pressure. Numerous investigations have confirmed the established link between dietary salt intake and hypertension. Reducing sodium in the diet is linked to lower rates of cardiovascular disease morbidity and mortality as well as lower rates of blood pressure and hypertension. In both human and animal research, high salt diets increase local and systemic tissue inflammation and compromise gut architecture. Given that the gut microbiota constantly interacts with the immune system and is required for the correct maturation of immune cells, it is scientifically conceivable that it mediates the inflammatory response. This review highlights the therapeutic possibilities for focusing on intestinal microbiomes as well as the potential functions of the gut microbiota and its metabolites in the development of hypertension.

Several studies revealed that synbiotics have been beneficial in managing non-alcoholic fatty liver disease (NAFLD), but the findings are conflicting. We aimed to assess the effect of synbiotic supplementation on cardiovascular risk factors in patients with NAFLD.

A thorough literature search was conducted to identify relevant studies up to July 2024, including publications from Pubmed, Embase, Cochrane, Scopus, and the Web of Science. Standardized mean difference (SMD) was used, and data with a 95% confidence interval (CI) were presented.

Sixteen RCTs were included, involving NAFLD patients and synbiotic supplementation. No significant effects were found on blood pressure (SBP: SMD - 6.68, p = 0.234; DBP: SMD - 4.31, p = 0.391), anthropometric measures (weight: SMD - 0.78, p = 0.126; BMI: SMD - 0.21, p = 0.182; waist circumference: SMD - 0.53, p = 0.095), or lipid profile (triglycerides: SMD - 3.67, p = 0.266; total cholesterol: SMD - 0.61, p = 0.059; low-density lipoprotein: SMD - 3.09, p = 0.215; high-density lipoprotein: SMD 0.49, p = 0.219). Synbiotics significantly reduced CRP levels (SMD - 1.83, p = 0.019) but had no significant effect on TNF-α (SMD - 1.95, p = 0.087). Synbiotic led to a significant reduction in weight following adjustment of publication bias (SMD - 1.16, p < 0.05).

Overall, synbiotic supplementation does not significantly impact blood pressure, anthropometric indices, or lipid profile parameters in patients with NAFLD, except for a significant reduction in weight after adjusting for publication bias. Synbiotic supplementation significantly reduces CRP levels but has no effect on TNF-α.

Experimental research on the link between unprocessed red meat and cardiovascular disease risk is inconsistent and may differ according to the financial interests of red meat industry sponsors.

This study aims to assess whether studies sponsorship or conflicts of interest with the red meat industry are associated with reported outcomes of unprocessed red meat consumption effect on risk factors for cardiovascular disease.

PubMed, Cochrane Library, and Scopus were searched from the inception of the databases to 3 March 2024. Studies were classified as "Red meat industry-related" if any of the authors declared affiliation or financial disclosure indicating a link to the red meat industry; or "Red Meat industry-independent." Reported outcomes were independently graded as favorable, neutral, or unfavorable. Studies were also categorized by type of control group. The quality of evidence for each outcome was evaluated using the Grading of Recommendations Assessment, Development and Evaluation approach.

A total of 44 studies were included, of which 66% had a link to the red meat industry. All independent studies reported either unfavorable (73.3%) or neutral (26.7%) cardiovascular outcomes when consuming unprocessed red meat. Conversely, all studies related to the red meat industry reported either favorable (20.7%) or neutral (79.3%) cardiovascular outcomes for red meat intake. A total of 69.6% of trials (16 of 23) showed a neutral effect of unprocessed red meat compared with other animal proteins, whereas 70% (7 of 10) reported an unfavorable effect compared with plant proteins. Studies with conflicts of interest were nearly 4 times more likely to report "Favorable/Neutral" outcomes compared with independent studies (odds ratio 3.75, 95% confidence interval: 1.62, 8.67).

Our findings highlight that using animal protein as a comparator in industry-funded studies, with quality of evidence rated as very low to low, may underestimate the cardiovascular benefits of reducing red meat intake. Most studies without conflicts of interest with the red meat industry suggested an unfavorable effect of unprocessed red meat consumption on risk factors for cardiovascular disease.

This trial for systematic reviews or meta-analyses was registered at PROSPERO as CRD42024525197 (https://www.crd.york.ac.uk/prospero/display_record.php?RecordID=525197).

The human body is habitat to a wide spectrum of microbial populations known as microbiota, which play an important role in overall health. The considerable research has mostly focused on the gut microbiota due to its potential to impact numerous physiological functions and its correlation with a variety of disorders, such as cardiovascular diseases (CVDs). Imbalances in the gut microbiota, known as dysbiosis, have been linked to the development and progression of CVDs through various processes, including the generation of metabolites like trimethylamine-N-oxide and short-chain fatty acids. Studies have also looked at the idea of using therapeutic interventions, like changing your diet, taking probiotics or prebiotics, or even fecal microbiota transplantation (FMT), to change the gut microbiota's make-up and how it works in order to prevent or treat CVDs. Exploring the cause-and-effect connection between the gut microbiota and CVDs offers a hopeful path for creating innovative microbiome-centered strategies to prevent and cure CVDs. This review presents an in-depth review of the correlation between the gut microbiota and CVDs, as well as potential therapeutic approaches for manipulating the gut microbiota to enhance cardiovascular health.

The role of the intestinal microbiota and its influence on neurodegenerative disorders has recently been extensively explored, especially in the context of Parkinson's disease (PD). In particular, its role in immunomodulation, impact on inflammation, and participation in the gut-brain axis are under ongoing investigations. Recent studies have revealed new data that could be important for exploring the neurodegeneration mechanisms connected with the gut microbiota, potentially leading to the development of new methods of treatment. In this review, the potential roles of the gut microbiota in future disease-modifying therapies were discussed and the properties of the intestinal microbiota-including its impacts on metabolism and short-chain fatty acids and vitamins-were summarized, with a particular focus on atypical Parkinsonian syndromes. This review focused on a detailed description of the numerous mechanisms through which the microbiota influences neurodegenerative processes. This review explored potentially important connections between the gut microbiota and the evolution and progression of atypical Parkinsonian syndromes. Finally, a description of recently derived results regarding the microbiota alterations in atypical Parkinsonian syndromes in comparison with results previously described in PD was also included.

Doxorubicin is a widely used chemotherapy for the treatment of several types of cancer. However, its application is restricted due to adverse effects, particularly cardiotoxicity, which can progress to heart failure-a chronic and debilitating condition. Several mechanisms have been identified in the pathophysiology of doxorubicin-induced cardiotoxicity, including oxidative stress, mitochondrial dysfunction, inflammation, and disruption of collagen homeostasis. More recently, dysbiosis of the gut microbiota has been implicated in the development and perpetuation of cardiac injury. Studies have reported alterations in the composition and abundance of the microbiota during doxorubicin treatment. Therefore, as of recent, there is a new field of research in order to develop strategies involving the gut microbiota to prevent or attenuate cardiotoxicity since there is no effective therapy at the moment. This narrative review aims to provide an update on the role of gut microbiota and intestinal permeability in the pathophysiology of cardiovascular diseases, and more specifically doxorubicin-induced cardiotoxicity. Additionally, it seeks to establish a foundation for future research targeting gut microbiota to alleviate cardiotoxicity.

Short-chain fatty acids (SCFAs), mainly produced by gut microbiota through the fermentation process of dietary fibers and proteins, are crucial to human health, with butyrate, a famous four-carbon SCFA, standing out for its inevitably regulatory impact on both gut and immune functions. Within this narrative review, the vital physiological functions of SCFAs were examined, with emphasis on butyrate's role as an energy source for colonocytes and its ability to enhance the gut barrier while exhibiting anti-inflammatory effects. Knowledge of butyrate synthesis, primarily generated by Firmicutes bacteria, can be influenced by diets with specifically high contents of resistant starches and fiber. Butyrate can inhibit histone deacetylase, modulate gene expression, influence immune functionality, and regulate tight junction integrity, supporting the idea of its role in gut barrier preservation. Butyrate possesses systemic anti-inflammatory properties, particularly, its capacity to reduce pro-inflammatory cytokines and maintain immune homeostasis, highlighting its therapeutic potential in managing dysbiosis and inflammatory diseases. Although butyrate absorption into circulation is typically minimal, its broader health implications are substantial, especially regarding obesity and type 2 diabetes through its influence on metabolic regulation and inflammation. Furthermore, this narrative review thoroughly examines butyrate's growing recognition as a modulator of neurological health via its interaction with the gut-brain axis. Additionally, butyrate's neuroprotective effects are mediated through activation of specific G-protein-coupled receptors, such as FFAR3 and GPR109a, and inhibition of histone deacetylases (HDACs). Research indicates that butyrate can alleviate neurological disorders, including Alzheimer's, Parkinson's, autism spectrum disorder, and Huntington's disease, by reducing neuroinflammation, enhancing neurotransmitter modulation, and improving histone acetylation. This focus will help unlock its full therapeutic potential for metabolic and neurological health, rather than exclusively on its well-known benefits for gut health, as these are often interconnected.

A microbiome in the gut plays a significant role in cardiovascular health and disease. Dysbiosis is an imbalance in the gut microbiome, leading to multiple cardiovascular diseases (CVD) such as atherosclerosis, hypertension, and heart failure. Gut microbe-derived metabolites such as trimethylamine-N-oxide (TMAO) and short-chain fatty acids (SCFAs) are important mediators of the gut-heart axis. Evaluation of the relationship between the gut microbiome and host biomarkers with CVD requires the integration of metagenomics and metabolomics with meta-omics approaches. The literature review found that microbes and metabolic signatures are associated with the risk and progression of CVD. The development of precision therapeutic approaches for targeting gut microbiota includes preventing adverse microbial effects using probiotics, prebiotics, and the drug-as-bug approach to inhibit harmful metabolites of microbiomes, and fecal microbiota transplantation (FMT). However, the implication and practice of these findings in clinical settings face challenges due to the heterogeneity of study designs, difficulty in the determination of causality, and the impact of confounding factors such as diet, medication, and potential inter-individual gut microbiome variability. Future researchers are recommended to conduct longitudinal studies to further establish both gut microbiome associations with CVD and develop successful precision therapeutics approaches based on the microbiome for the treatment of CVD.

Chronic Heart Failure (CHF) is one of the leading cardiovascular diseases (CVDs), particularly in the Asian population. Individuals with specific health risks, such as obesity, type 2 diabetes, hypertension, dyslipidemia, and coronary artery disease (CAD), are more susceptible to developing CHF. Current evidence is limited to understanding the link between gut microbiota dysbiosis and CHF. Therefore, this review aims to explore the potential connection between dietary patterns, gut microbiota, and its metabolites in individuals at risk of CHF in the Asian population.

A literature review of cross-sectional studies was conducted using primary keywords such as "Asian", "obesity", "type 2 diabetes", "hypertension", "dyslipidemia", "coronary artery disease", and "chronic heart failure". There was no restriction on sample size.

Several gut microbiotas were found to correlate with CHF risk factors. There were increased levels of Prevotella, Klebsiella, Romboutsia, Catenibacterium, Clostridium, Holdemanella, Ruminococcus, Coprococcus, Parabacteroides, Bacteroides, Lachnoclostridium, Streptococcus, and Megamonas, while decreased levels of Oscillibacter, Bifidobacterium, Lactobacillus, Akkermansia, Roseburia, Faecalibacterium, Pseudobutyrivibrio, and Eubacterium were reported. These microbiota shifts were linked to increased TMAO production and impaired short-chain fatty acids (SCFAs) production. Dietary intake and microbial metabolites were also identified as contributors to the gut microbiota associated with CHF.

A potential link exists between the gut microbiota profile and CHF risk factors, possibly mediated by microbial metabolites. Dietary patterns may influence CHF-associated gut microbiota and me-tabolites. Future research is needed to investigate how dietary modifications can modulate gut microbiota and its metabolites in CHF patients.

The application of fecal microbiota transplantation (FMT) as a therapeutic strategy to directly modify the makeup of the gut microbiota has made significant progress in the last few decades. The gut microbiota, a sizable microbial community present in the human gut, is essential for digestion, immunomodulation, and nutrition absorption. Alternatively, a growing body of research indicates that gut microbiota is a key contributor to cancer, and intratumoral bacteria are considered to be crucial "accomplices" in the development and metastasis of malignancies. The exceptional clinical effectiveness of FMT in treating melanoma patients has been adequately established in earlier research, which has created new avenues for the diagnosis and treatment of cancer and sparked an increasing interest in the treatment and prevention of other cancers. However, further research on the function and mechanisms of the gut microbiota is required to properly comprehend the impact and role of these organisms in tumor regulation. In this article, we present a detailed account of the influence of FMT on the entire course of cancer patients' illness and treatment, from tumor development, metastasis, and invasion, to the impact and application of treatment and prognosis, as well as address the associated mechanisms.

Cardiovascular-kidney-metabolic (CKM) syndrome represents a complex interplay between cardiovascular disease (CVD), chronic kidney disease (CKD), and metabolic disorders, significantly impacting cancer patients. The presence of CKM syndrome in cancer patients not only worsens their prognosis but also increases the risk of major adverse cardiovascular events (MACE), reduces quality of life (QoL), and affects overall survival (OS). Furthermore, several anticancer therapies, including anthracyclines, tyrosine kinase inhibitors, immune checkpoint inhibitors, and hormonal treatments, can exacerbate CKM syndrome by inducing cardiotoxicity, nephrotoxicity, and metabolic dysregulation. This review explores the pathophysiology of CKM syndrome in cancer patients and highlights emerging therapeutic strategies to mitigate its impact. We discuss the role of novel pharmacological interventions, including sodium-glucose cotransporter-2 inhibitors (SGLT2i), proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i), and soluble guanylate cyclase (sGC) activators, as well as dietary and lifestyle interventions. Optimizing the management of CKM syndrome in cancer patients is crucial to improving OS, enhancing QoL, and reducing MACE. By integrating cardiometabolic therapies into oncologic care, we can create a more comprehensive treatment approach that reduces the burden of cardiovascular and renal complications in this vulnerable population. Further research is needed to establish personalized strategies for CKM syndrome prevention and treatment in cancer patients.

Several anthropometric indices, such as body mass index and waist circumference, have been used as clinical screening tools for the prediction of nonalcoholic fatty liver disease (NAFLD). To further refine these clinical tools for NAFLD, the body roundness index (BRI) has recently been evaluated. In this systematic review and meta-analysis, the objective was to evaluate the relationship and predictive capability of the BRI in identifying NAFLD.

A comprehensive search was conducted in PubMed, Embase, Web of Science, and Scopus up to December 31, 2024. Eligibility criteria included observational studies on adults (≥ 18 years old) with measured BRI and its association with NAFLD. The Joanna Briggs Institute tool was used for risk of bias assessment. Meta-analyses used random-effects models to pool data on mean difference, odds ratio, sensitivity, specificity, and the area under the curve (AUC), with heterogeneity and publication bias assessed.

Ten studies involving 59,466 participants were included. The pooled mean difference in BRI between the NAFLD and non-NAFLD groups was 1.73 (95% confidence interval [CI]: 1.31-2.15). The pooled sensitivity and specificity of BRI for diagnosing NAFLD were 0.806 and 0.692, respectively. The pooled AUC for BRI was 0.803 (95% CI: 0.775-0.830), indicating good diagnostic accuracy. Unlike subgroup analysis by country, subgroup analysis by sex showed no significant differences. Higher BRI values were associated with increased odds of NAFLD (pooled OR = 2.87, 95% CI: 1.39; 5.96). Studies provided mixed results on the predictive ability of BRI compared to other indices like body mass index, mostly favoring BRI over conventional indices.

BRI demonstrates a good diagnostic performance for NAFLD, suggesting it may be a valuable clinical tool for NAFLD assessment. Further research is necessary to validate these findings and strengthen the evidence base.

Autism spectrum disorder (ASD) is a group of complex neurodevelopmental conditions with a heterogeneous and multifactorial etiology that is not yet fully understood. Among the various factors that may contribute to ASD development, alterations in the gut microbiota have been increasingly recognized. Microorganisms in the gastrointestinal tract play a crucial role in the gut-brain axis (GBA), affecting nervous system development and behavior. Dysbiosis, or an imbalance in the microbiota, has been linked to both behavioral and gastrointestinal (GI) symptoms in individuals with ASD. The microbiota interacts with the central nervous system through mechanisms such as the production of short-chain fatty acids (SCFAs), the regulation of neurotransmitters, and immune system modulation. Alterations in its composition, including reduced diversity or an overabundance of specific bacterial taxa, have been associated with the severity of ASD symptoms. Dietary modifications, such as gluten-free or antioxidant-rich diets, have shown potential for improving gut health and alleviating behavioral symptoms. Probiotics, with their anti-inflammatory properties, may support neural health and reduce neuroinflammation. Fecal microbiota transplantation (FMT) is being considered, particularly for individuals with persistent GI symptoms. It has shown promising outcomes in enhancing microbial diversity and mitigating GI and behavioral symptoms. However, its limitations should be considered, as discussed in this narrative review. Further research is essential to better understand the long-term effects and safety of these therapies. Emphasizing the importance of patient stratification and phenotype characterization is crucial for developing personalized treatment strategies that account for individual microbiota profiles, genetic predispositions, and coexisting conditions. This approach could lead to more effective interventions for individuals with ASD. Recent findings suggest that gut microbiota may play a key role in innovative therapeutic approaches to ASD management.

The intestinal flora (IF) has been linked to risks of non-communicable diseases, especially various cancers, stroke, and Alzheimer's disease. However, many uncertainties of these associations during different stages of growth, development, and aging still exist. Therefore, further in-depth explorations are warranted.

To explore the associations of the human IF with disease risks during different stages of growth, development, and aging to achieve more accurate and convincing conclusions.

Cohort, cross-sectional, case-control, and Mendelian randomization studies published in the PubMed and Web of Science databases until December 31, 2023 were systematically reviewed to clarify the associations of the IF at the genus level with the risks of various non-communicable diseases, which were grouped in accordance with the 10th revision of the International Classification of Diseases.

In total, 57 studies were included to quantitatively examine the influence of the IF on the risks of 30 non-communicable diseases during different stages of growth, development, and aging. Population studies and Mendelian randomization studies confirmed positive associations of the abundances of Bifidobacterium and Ruminococcus with multiple sclerosis.

These findings contribute to a deeper understanding of the roles of the IF and provide novel evidence for effective strategies for the prevention and treatment of non-communicable diseases. In the future, it will be necessary to explore a greater variety of research techniques to uncover the specific mechanisms by which gut microbiota trigger diseases and conduct in-depth studies on the temporal relationship between microbiota alterations and diseases, so as to clarify the causal relationship more accurately.

The gut microbiome comprises a vast community of microbes inhabiting the human alimentary canal, playing a crucial role in various physiological functions. These microbes generally live in harmony with the host; however, when dysbiosis occurs, it can contribute to the pathogenesis of diseases, including osteoporosis. Osteoporosis, a systemic skeletal disease characterized by reduced bone mass and increased fracture risk, has attracted significant research attention concerning the role of gut microbes in its development. Advances in molecular biology have highlighted the influence of gut microbiota on osteoporosis through mechanisms involving immunoregulation, modulation of the gut-brain axis, and regulation of the intestinal barrier and nutrient absorption. These microbes can enhance bone mass by inhibiting osteoclast differentiation, inducing apoptosis, reducing bone resorption, and promoting osteoblast proliferation and maturation. Despite these promising findings, the therapeutic effectiveness of targeting gut microbes in osteoporosis requires further investigation. Notably, gut microbiota has been increasingly studied for their potential in early diagnosis, intervention, and as an adjunct therapy for osteoporosis, suggesting a growing utility in improving bone health. Further research is essential to fully elucidate the therapeutic potential and clinical application of gut microbiome modulation in the management of osteoporosis.

The delivery of biomolecules to target cells has been a longstanding challenge in biotechnology. DNA viruses naturally evolved the ability to deliver genetic material to cells and modulate cellular processes. As such, they inherently possess requisite characteristics that have led to their extensive study, engineering, and development as biotechnological tools. Here, we overview the application of DNA viruses to biotechnology, with specific implications in basic research, health, biomanufacturing, and agriculture. For each application, we review how an increasing understanding of virology and technological methods to genetically manipulate DNA viruses has enabled advances in these fields. Additionally, we highlight the remaining challenges to unlocking the full biotechnological potential of DNA viral technologies. Finally, we discuss the importance of balancing continued technological progress with ethical and biosafety considerations.

Atrial fibrillation (AF) is a prevalent clinical arrhythmia associated with a high incidence and severe complications such as cerebral embolism and heart failure. While the etiology and pathogenesis of AF involve numerous factors, recent research emphasizes the significant role of intestinal microbiota imbalance in the emergence and progression of AF, particularly among older adults. This review investigates the mechanisms by which intestinal flora and their metabolites contribute to the onset of AF in the elderly, highlighting novel interactions between gut health and cardiac function. Current literature often overlooks these critical connections, indicating a substantial research gap in understanding how dysbiosis may exacerbate AF and hinder recovery. Furthermore, exploring the bidirectional relationship between the gut microbiome and systemic inflammation in the context of AF provides a unique perspective that has yet to be thoroughly investigated. Future research should focus on longitudinal studies assessing gut microbiota composition and function in AF patients and consider probiotics or prebiotics as potential adjunctive therapies for mitigating AF. This comprehensive approach may pave the way for innovative treatments integrating cardiology with gastroenterology, enhancing patient outcomes through a holistic understanding of health.

To examine the associations between unhealthy alcohol use and risk of coronary heart disease (CHD) among women and men aged 18-65 years.

An observational study in an integrated healthcare system with systematic alcohol screening. We identified 432,265 primary care patients aged 18-65 years who, in 2014-2015, reported weekly alcohol intake levels. Weekly alcohol intake, categorized into below (≤14/week men; ≤7/week women) and above limits (≥15/week men; ≥ 8/week women) per U.S. guidelines, and heavy episodic drinking (HED, ≥5/≥4 drinks any day in past 3 months for men/women, respectively). Main outcome was CHD during 4-year follow-up, based on inpatient ICD diagnoses of myocardial infarction and CHD. Cox proportional hazards models adjusted for age, sex, race/ethnicity, body mass index, physical activity, smoking, hypertension, diabetes, and hyperlipidemia.

The cohort comprised 44 % women, mean age (standard deviation) of 43.5 years (±13.1). Weekly alcohol intake above limits was associated with higher prevalence of cardiovascular risk factors, and a 26 %, 19 % and 43 % higher risk on the overall, men- and women-specific risk of CHD after adjusting for these risk factors (hazard ratio [95 % confidence interval] = 1.26[1.13 -1.40], 1.19[1.04-1.35] and 1.43[1.20-1.71], respectively).

In a large, real-world, diverse population with a systematic alcohol screening program, having weekly alcohol intake above limits was associated with increased risk of CHD among young and middle-aged men and women. Increased CHD risk due to alcohol intake above limits warrants particular awareness and interventions.

Current studies suggest a potential link between inflammatory bowel disease (IBD), comprising Crohn's disease (CD) and ulcerative colitis (UC), and cardiovascular diseases, such as stroke. This study aimed to assess the risk of stroke in IBD patients compared to general population.

Systematic search was done in PubMed, Embase, CENTRAL, Scopus, and CINAHL databases for studies published till September 2023. Using a random-effects model, the hazard ratios (HRs) with 95% confidence intervals (CIs) for stroke occurrence were calculated. Subgroup analyses were done to estimate pooled HR with 95%CI for CD, UC, and overall IBD cases separately. Publication bias assessment was done by Begg's and Egger's tests.

Thirteen studies with 2,802,955 participants were included. IBD patients in general had significantly higher risk of stroke, with HR of 1.30 [95% CI 1.21-1.39]. Subgroup analysis demonstrated an HR of 1.35 [95% CI 1.22-1.49] for CD and 1.15 [95% CI 1.09-1.22] for UC. Substantial heterogeneity was detected across studies, with no substantial publication bias. Sensitivity analyses affirmed the stability of findings.

IBD in general, and Crohn's disease in particular are associated with significantly higher risk of stroke. Our findings further emphasize the importance of cardiovascular risk assessment and management strategies in IBD care.

PROSPERO, CRD42023470602.

Trimethylamine N-oxide (TMAO) is a product of the action of gut microbiota on choline and other choline-containing compounds ingested in the diet. The presence of TMAO at high concentrations has been reported in the blood of patients with cardiovascular disease, suggesting the role for TMAO as either a marker or causative agent of the disease. These investigations examined whether TMAO had an effect on cardiomyocyte contractile function, calcium homoeostasis, and survival from metabolic insult.

TMAO had no effect on metabolic function or the ability of cells to survive a metabolic insult; however, it did cause transient changes to contractile function. These changes included an increase in calcium current and an increase in Kir6.1 channel activity in the cell, causing a shortening of the action potential duration to 90% repolarised but lengthening the action potential to 30% repolarised. These effects occurred within minutes of TMAO application; however, they were not observed following 24 h culture. These data suggest that TMAO does modulate contractile function, albeit only in the short-term, but has no effect on metabolic behaviour or the ability to withstand a metabolic challenge.

These data suggest that high TMAO concentrations in the blood of patients may be a marker of potential cardiovascular disease rather than playing a causative role.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterised by lipid accumulation in the liver and is often associated with obesity and type 2 diabetes. The gut microbiome recently emerged as a significant player in liver metabolism and health. Hippurate, a host-microbial co-metabolite has been associated with human gut microbial gene richness and with metabolic health. However, its role on liver metabolism and homeostasis is poorly understood.

We characterised liver biospies from 318 patients with obesity using RNAseq and metabolomics in liver and plasma to derive associations among hepatic hippurate, hepatic gene expression and MASLD and phenotypes. To test a potential beneficial role for hippurate in hepatic insulin resistance, we profile the metabolome of (IHH) using ultra-high-performance liquid chromatography coupled to high-resolution tandem mass spectrometry (UHPLC-MS/MS), and characterised intracellular triglyceride accumulation and glucose internalisation after a 24 h insulin exposure.

We first report significant associations among MASLD traits, plasma and hepatic hippurate. Further analysis of the hepatic transcriptome shows that liver and plasma hippurate are inversely associated with MASLD, implicating lipid metabolism and regulation of inflammatory responses pathways. Hippurate treatment inhibits lipid accumulation and rescues insulin resistance induced by 24-hour chronic insulin in IHH. Hippurate also improves hepatocyte metabolic profiles by increasing the abundance of metabolites involved in energy homeostasis that are depleted by chronic insulin treatment while decreasing those involved in inflammation.

Altogether, our results further highlight hippurate as a mechanistic marker of metabolic health, by its ability to improve metabolic homeostasis as a postbiotic candidate.

Improving gut dysbiosis and impaired gut-brain axis has been a potent therapeutic strategy for treating myocardial infarction (MI). Geniposide (GEN), a traditional Chinese medicine extract, has demonstrated substantial cardioprotective properties post-MI. Nevertheless, the effect of GEN on gut microbial, gut-brain communication, and its potential mechanism remains unclear. In this study, we initially found that GEN significantly alleviated MI-induced cardiac dysfunction from echocardiographic data and decreased myocardial fibrosis, inflammation, apoptosis and hypertrophy post-MI. Additionally, we investigated the effects of GEN on gut pathology, and observed that GEN led to a remarkable change in gut microbiota as evidenced by altering β-diversity and short-chain fatty acids (SCFAs) levels, and alleviated intestinal damage indicated by reduced inflammation and barrier permeability post-MI. Finally, our investigation into brain pathology revealed that GEN induced a remarkable inhibition in PVN inflammation and sympathetic activity following MI. Collectively, these findings imply that the cardioprotective effects of GEN against MI were mediated possibly via an improvement in the impaired gut-brain axis. Mechanically, GEN-induced increase of microbiota-derived SCFAs might be the critical factor linking gut microbiota and reduced neuroinflammation with PVN, which leads to the suppression of sympathetic activation, therefore protecting the myocardium against MI-induced damage.

Stachydrine (STA) has therapeutic effects on heart disorders. The current study assessed its effects on Type 2 diabetes (T2D) induced cardiac disorders by focusing on the heart-gut axis. Mice were subjected to high-fat diet (HFD) and streptozocin (STZ) to induce cardiac disorders such as inflammation and structural deteriorations, which were handled with STA. Changes regarding the composition and metabolism of gastrointestinal (GI) microbiota were then determined using a multiomics strategy, including amplicon sequencing and metabolomics. The data showed that STA improved heart function, reduced intestinal permeability, and suppressed inflammation in mice in a dose-dependent manner. However, the compound had little influence on the overall alpha diversity of gut microbiota, while it did influence the beta diversity. The analyses based on the multiomics strategy demonstrated that certain GI microbial groups, including Paramuribaculum, Allobaculum, Bifidobacterium, and Adlercreutzia, responded to the STA administration, which contributed to the alternatives of metabolites in the gut. Correlation analyses showed that Duncaniella and Ruminococcus negatively impacted health, while Muribaculum, Paramuribaculum, and Prevotella positively influenced intestinal permeability and heart health. Collectively, STA attenuated T2D-induced cardiac disorders by improving heart structure and function and suppressing inflammation, during which the GI homeostasis of the T2D mice changed to an alternative state that was different from that of healthy mice.

Heart failure (HF) is a complex syndrome marked by considerable expenditures and elevated mortality and morbidity rates globally. Shenmai injection (SMI), a form of Traditional Chinese Medicine-based therapy, has demonstrated effectiveness in treating HF. Recent research suggests that Traditional Chinese Medicine (TCM) may induce beneficial changes in microbial-host co-metabolism, potentially providing cardiovascular protection. This study used a rat model of hypertensive heart failure (H-HF) to explore the mechanism of SMI. The possible compounds and key targets of SMI against H-HF were investigated using network pharmacology. The pharmacodynamics of SMI were validated using the H-HF animal model, with analysis of fecal gut microbiota integrating metabolomics and 16S rRNA sequencing. Metorigin metabolite traceability analysis and the MetaboAnalyst platform were utilized to explore the action mechanism. To evaluate changes in serum TMAO levels, targeted metabolomics was performed. Finally, the study looked at the intrinsic relationships among modifications in the intestinal flora, metabolite profile changes, and the targets of SMI compounds to clarify how they might be used to treat H-HF. According to metabolomics and 16S rRNA sequencing, by reestablishing homeostasis in the gut microbiota, SMI affects vital metabolic pathways, such as energy metabolism, amino acid metabolism, and bile acid metabolism. Increased serum TMAO levels were identified to be a risk factor for H-HF, and SMI was able to downregulate the levels of TMAO-related metabolites. Network pharmacology analysis identified 13 active components of SMI targeting 46 proteins, resulting in differential expression changes in 8 metabolites and 24 gut microbes. In conclusion, this study highlights the effectiveness of SMI in alleviating H-HF and its potential to modulate microbial-host co-metabolism. Through a comprehensive discussion of the interconnected relationships among the components, targets, metabolites, and gut microbiota, it provided fresh light on the therapeutic mechanism of SMI on H-HF.

This study aimed to evaluate the effectiveness of Internet-based Cognitive Behavioral Therapy (ICBT) in reducing anxiety and depressive symptoms among patients with cardiovascular diseases (CVDs) and to explore how intervention characteristics, such as module number and program duration, influence treatment outcomes.

A systematic review and meta-analysis were conducted by searching eight databases, including PubMed, Embase, and Cochrane Library, for randomized controlled trials (RCTs) published up to December 2023. Studies involving adult CVD patients with anxiety or depressive symptoms who underwent ICBT interventions were included. Statistical analyses used random-effects models, with subgroup analyses performed to assess the impact of intervention format, module number, and program duration. Sensitivity and publication bias assessments ensured the robustness of the findings.

Eight RCTs with 1177 participants were included. ICBT significantly reduced depressive symptoms (SMD = -0.32, 95% CI [-0.56, -0.08], p < 0.015) and anxiety symptoms (SMD = -0.37, 95% CI [-0.68, -0.06], p < 0.001). Subgroup analysis indicated that self-guided ICBT was more effective than therapist-guided ICBT. Programs with fewer than eight modules were more effective for anxiety, while those with eight or more modules were more effective for depression. Shorter programs (< 9 weeks) were better for anxiety, whereas longer programs (≥ 9 weeks) were more effective for depression.

ICBT is an effective intervention for managing anxiety and depression in CVD patients. Tailoring ICBT interventions based on symptom type, module number, and program duration can optimize outcomes. Future research should explore personalized, long-term strategies to enhance effectiveness and safety.

Cardiovascular diseases (CVDs) present differently in women and men, influenced by host-microbiome interactions. The roles of sex hormones in CVD outcomes and gut microbiome in modifying these effects are poorly understood. The XCVD study examines gut microbiome mediation of sex hormone effects on CVD risk markers by observing transgender participants undergoing gender-affirming hormone therapy (GAHT), with findings expected to extrapolate to cisgender populations.

This observational, longitudinal cohort study includes baseline, 1- and 2-year follow-ups with transgender participants beginning GAHT. It involves comprehensive phenotyping and microbiome genotyping, integrating computational analyses of high-dimensional data. Microbial diversity will be assessed using gut, skin, and oral samples via 16S rRNA and shotgun metagenomic sequencing of gut samples. Blood measurements will include sex hormones, CVD risk markers, cardiometabolic parameters, cytokines, and immune cell counts. Hair samples will be analysed for cortisol. Participants will complete online questionnaires on physical activity, mental health, stress, quality of life, fatigue, sleep, pain, and gender dysphoria, tracking medication use and diet to control for confounders. Statistical analyses will integrate phenomic, lifestyle, and multi-omic data to model health effects, testing gut microbiome mediation of CVD risk as the endocrine environment shifts between that typical for cisgender men to women and vice versa.

The study adheres to Good Clinical Practice and the Declaration of Helsinki. The protocol was approved by the Charité Ethical Committee (EA1/339/21). Signed informed consent will be obtained. Results will be published in peer-reviewed journals and conferences and shared as accessible summaries for participants, community groups, and the public, with participants able to view their data securely after public and patient involvement review for accessibility.

The XCVD study was registered on ClinicalTrials.gov (NCT05334888) as 'Sex-differential host-microbiome CVD risk - a longitudinal cohort approach (XCVD)" on 4 April 2022. Data set link can be found at https://classic.

gov/ct2/show/NCT05334888.

Cardiovascular diseases (CVDs) are a major cause of morbidity and mortality worldwide and there are strong links existing between gut health and cardiovascular health. Gut microbial diversity determines gut health. Dysbiosis, described as altered gut microbiota, causes bacterial translocations and abnormal gut byproducts resulting in systemic inflammation.

To review the current literature on the relationships between gut microbiota, dysbiosis, and CVD development, and explore therapeutic methods to prevent dysbiosis and support cardiovascular health.

Dysbiosis increases levels of pro-inflammatory substances while reducing those of anti-inflammatory substances. This accumulative inflammatory effect negatively modulates the immune system and promotes vascular dysfunction and atherosclerosis. High Firmicutes to Bacteroidetes ratios, high trimethylamine-n-oxide to short-chain fatty acid ratios, high indole sulfate levels, low cardiac output, and polypharmacy are all associated with worse cardiovascular outcomes. Supplementation with prebiotics and probiotics potentially alleviates some CVD risk. Blood and stool samples may be used in clinical practice to quantify and qualify gut bacterial ratios and byproducts, assess patients' risk for adverse cardiovascular outcomes, and track their gut health progress. Further research is required to set population-based cutoffs for normal and abnormal gut microbiota and byproduct ratios.

The pathophysiology of cardiovascular diseases encompasses a complex interplay of genetic and environmental risk factors. Even if traditional risk factors are treated to target, there remains a residual risk.

This manuscript reviews the potential role of gut microbiota in the development of cardiovascular disease, and as potential target. A systematic search was conducted until 30 October 2024 on PubMed (MEDLINE), using the MeSH terms [Gut microbiota] + [Dysbiosis] + [Cardiovascular] + [TMAO] + [bile acids] + [short-chain fatty acids].

The term dysbiosis implies changes in equilibrium, with modifications in the composition and functionality of microbiota and a series of additional factors: reduced diversity and uniformity of microorganisms; reduced short-chain fatty acid-producing bacteria; increased gut permeability; release of metabolites, such as trimethylamine N-oxide, betaine, phenylalanine, tryptophan-kynurenine, phenylacetylglutamine, and lipopolysaccharides; and reduced secondary bile acid excretion, leading to inflammation, oxidative stress, and endothelial dysfunction and facilitating the onset of pathological conditions, including obesity, hypertension, diabetes, atherosclerosis, and heart failure. Attempts to restore gut microbiota balance through different interventions, mainly changes in diet, have been shown to positively affect individual components and metabolites and reduce the risk of cardiovascular disease. In addition, probiotics and prebiotics are potentially useful. Fecal microbiota transplantation is a promising therapy.

The relationship between gut microbiota composition and the development of cardiovascular disease, with a potential role of microbial metabolites in inflammatory and metabolic pathways is of interest. We analyzed gut microbiota and markers of cardiovascular health in a cohort of 100 participants for three years to search for microbial signatures correlated with increased CVD risk. Our results show several correlations between specific microbial taxa, lipid metabolism and systemic inflammation, whereby a higher Firmicutes/Bacteroides ratio is associated with a greater incidence of CVD. These results suggest that intervention targeting the microbiome has the potential to reduce risk for CVD and point towards a role for gut microbiota in cardiovascular health.

Atrial fibrillation (AF) is the most frequent arrhythmia in the adult population associated with a high rate of severe consequences leading to significant morbidity and mortality worldwide. Therefore, its prompt recognition is of high clinical importance. AF detection often remains challenging due to unspecific symptoms and a lack of reliable biomarkers for its prediction. Herein, novel bioanalytical methodologies, such as metabolomics, offer new opportunities for a better understanding of the underlying pathological mechanisms of cardiovascular diseases, including AF. The metabolome, considered a complete set of small molecules present in the organism, directly reflects the current phenotype of the studied system and is highly sensitive to any changes, including arrhythmia's onset. A growing body of evidence suggests that metabolite profiling has prognostic value in AF prediction, highlighting its potential role not only in early diagnosis but also in guiding therapeutic interventions. By identifying specific metabolites as a disease biomarker or recognising particular metabolomic pathways involved in the AF pathomechanisms, metabolomics could be of great clinical value for further clinical decision-making, risk stratification, and an individual personalised approach. The presented narrative review aims to summarise the current state of knowledge on metabolomics in AF with a special emphasis on its implications for clinical practice and personalised medicine.

This study aimed to explore the changes in gut microbiota and its metabolites in different pathophysiological stages of doxorubicin (DOX)-induced heart failure (DIHF) and the relationship between gut microbiota and metabolites in various degrees of DIHF.

C57BL/6 J mice were injected intraperitoneally with 5 mg/kg of DOX once a week for 5 consecutive weeks. At different times after injection, the cardiac function and histopathological analysis was conducted, the serum levels of creatine kinase (CK), CK-MB, lactic dehydrogenase, and cardiac troponin T were determined. 16S rRNA gene sequencing of feces and the nontargeted metabolomics analysis of serum were performed. Multi-omics analyses were used to explore the correlation between gut microbiota and serum metabolites.

The results showed that DOX caused cardiac contractile dysfunction and left ventricular (LV) dilation. The levels of myocardial enzymes significantly increase in 3 and 5 weeks after DOX injection. DOX-treated mice showed significant differences in the composition and abundance of gut microorganisms, and the levels of serum metabolites at different times of treatment. Multi-omics analyses showed that intestinal bacteria were significantly correlated with the differential metabolites. Some bacteria and metabolites can be used as biomarkers of DIHF (AUC > 0.8). KEGG analyses showed the involvement of different metabolic pathways in various degrees of DIHF.

Marked differences were found in the composition and abundance of gut microorganisms, the levels of serum metabolites and metabolic pathways in different degrees of DIHF. The intestinal bacteria were significantly correlated with differential metabolites in different degrees of DIHF. The gut microbiota may serve as new targets for the treatment of DIHF.

Hypertension is a common disease; however, it is more prevalent in older adults, and its prevalence is increasing in younger populations. Numerous studies have revealed that hypertension and the composition and functionality of the intestinal flora are closely correlated. The balance of the intestinal flora, intestinal barrier integrity, and metabolite content of the intestinal flora play significant roles in the occurrence and progression of hypertension. Therefore, we performed a comprehensive review of Traditional Chinese medicine (TCM) for hypertension, focusing on the role of the intestinal flora to understand the mechanism by which TCM regulates hypertension through its effects on the intestinal flora. We analyzed the findings using the terms "traditional Chinese medicine," "hypertension," "high blood pressure," "blood pressure," "intestinal flora," "intestinal barrier function," "intestinal flora metabolites," and other keywords from the China National Knowledge Infrastructure, VIP Chinese Science and Technology, Wanfang Data, PubMed, and ScienceDirect databases. We found that TCM treats hypertension by regulating the balance of the intestinal microbiota, increasing the abundance of beneficial bacteria, reducing the abundance of harmful bacteria, improving intestinal barrier function, increasing compact proteins, reducing intestinal permeability, and regulating the content of intestinal flora metabolites. The use of TCM to treat hypertension by regulating the intestinal flora is a promising therapeutic strategy. However, most studies are limited by small sample sizes and there is a lack of large-scale randomized controlled trials. In the future, multi-center controlled clinical trials are needed to verify the efficacy and safety of TCM, optimize therapeutic protocols, and establish a foundation for the standardized and personalized application of TCM in hypertension management.

Alzheimer's Disease (AD) is a neurodegenerative disorder marked by cognitive decline, for which effective treatments remain elusive due to complex pathogenesis. Recent advances in neuroimaging, gene therapy, and gut microbiota research offer new insights and potential intervention strategies. Neuroimaging enables early detection and staging of AD through visualization of biomarkers, aiding diagnosis and tracking of disease progression. Gene therapy presents a promising approach for modifying AD-related genetic expressions, targeting amyloid and tau pathology, and potentially repairing neuronal damage. Furthermore, emerging evidence suggests that the gut microbiota influences AD pathology through the gut-brain axis, impacting inflammation, immune response, and amyloid metabolism. However, each of these technologies faces significant challenges, including concerns about safety, efficacy, and ethical considerations. This article reviews the applications, advantages, and limitations of neuroimaging, gene therapy, and gut microbiota research in AD, with a particular focus on their combined potential for early diagnosis, mechanistic insights, and therapeutic interventions. We propose an integrated approach that leverages these tools to provide a multi-dimensional framework for advancing AD diagnosis, treatment, and prevention.

Myocardial infarction (MI) is a lethal cardiovascular disease worldwide. Emerging evidence has revealed the critical role of gut dysbiosis and impaired gut-brain axis in the pathological progression of MI. Tanshinone IIA (Tan IIA), a traditional Chinese medicine, has been demonstrated to exert therapeutic effects for MI. However, the effects of Tan IIA on gut-brain communication and its potential mechanisms post-MI are still unclear. In this study, we initially found that Tan IIA significantly reduced myocardial inflammation, apoptosis and fibrosis, therefore alleviating hypertrophy and improving cardiac function following MI, suggesting the cardioprotective effect of Tan IIA against MI. Additionally, we observed that Tan IIA improved the gut microbiota as evidenced by changing the α-diversity and β-diversity, and reduced histopathological impairments by decreasing inflammation and permeability in the intestinal tissues, indicating the substantial improvement of Tan IIA in gut function post-MI. Lastly, Tan IIA notably reduced lipopolysaccharides (LPS) level in serum, inflammation responses in paraventricular nucleus (PVN) and sympathetic hyperexcitability following MI, suggesting that restoration of Tan IIA on MI-induced brain alterations. Collectively, these results indicated that the cardioprotective effects of Tan IIA against MI might be associated with improvement in gut-brain axis, and LPS might be the critical factor linking gut and brain. Mechanically, Tan IIA-induced decreased intestinal damage reduced LPS release into serum, and reduced serum LPS contributes to decreased neuroinflammation with PVN and sympathetic inactivation, therefore protecting the myocardium against MI-induced injury.

In recent years, there has been a surge in the popularity of fasting as a method to enhance one's health and overall well-being. Fasting is a customary practice characterized by voluntary refraining from consuming food and beverages for a specified duration, ranging from a few hours to several days. The potential advantages of fasting, including enhanced insulin sensitivity, decreased inflammation, and better cellular repair mechanisms, have been well documented. However, the effects of fasting on cancer therapy have been the focus of recent scholarly investigations. Doxorubicin (Dox) is one of the most widely used chemotherapy medications for cancer treatment. Unfortunately, cardiotoxicity, which may lead to heart failure and other cardiovascular issues, has been linked to Dox usage. This study aims to comprehensively examine the possible advantages and disadvantages of fasting concerning Dox-induced cardiotoxicity. Researchers have investigated the potential benefits of fasting in lowering the risk of Dox-induced cardiac damage to solve this problem. Nevertheless, new studies indicate that prolonged alternate-day fasting may adversely affect the heart's capacity to manage the cardiotoxic properties of Dox. Though fasting may benefit overall health, it is essential to proceed cautiously and consider the potential risks in certain circumstances.

The gut microbiota (GM) plays a critical role in regulating human physiology, with dysbiosis linked to various diseases, including heart failure (HF). HF is a complex syndrome with a significant global health impact, as its incidence doubles with each decade of life, and its prevalence peaks in individuals over 80 years. A bidirectional interaction exists between GM and HF, where alterations in gut health can worsen the disease's progression.

The "gut hypothesis of HF" suggests that HF-induced changes, such as reduced intestinal perfusion and altered gut motility, negatively impact GM composition, leading to increased intestinal permeability, the release of GM-derived metabolites into the bloodstream, and systemic inflammation. This process creates a vicious cycle that further deteriorates heart function. GM-derived metabolites, including trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), and secondary bile acids (BAs), can influence gene expression through epigenetic mechanisms, such as DNA methylation and histone modifications. These epigenetic changes may play a crucial role in mediating the effects of dysbiotic gut microbial metabolites, linking them to altered cardiac health and contributing to the progression of HF. This process is particularly relevant in older individuals, as the aging process itself has been associated with both dysbiosis and cumulative epigenetic alterations, intensifying the interplay between GM, epigenetic changes, and HF, and further increasing the risk of HF in the elderly.

Despite the growing body of evidence, the complex interplay between GM, epigenetic modifications, and HF remains poorly understood. The dynamic nature of epigenetics and GM, shaped by various factors such as age, diet, and lifestyle, presents significant challenges in elucidating the precise mechanisms underlying this complex relationship. Future research should prioritize innovative approaches to overcome these limitations. By identifying specific metabolite-induced epigenetic modifications and modulating the composition and function of GM, novel and personalized therapeutic strategies for the prevention and/or treatment of HF can be developed. Moreover, targeted research focusing specifically on older individuals is crucial for understanding the intricate connections between GM, epigenetics, and HF during aging.

Arterial hypertension is a major contributor to a wide range of health complications, with cardiac hypertrophy and chronic kidney disease being among the most prevalent. Consequently, novel strategies for the treatment and prevention of hypertension are actively being explored. Recent research has highlighted a potential link between hypertension and the gut-brain axis. A bidirectional communication between the microbiota and the brain via the vagus nerve, enteric nervous system, hypothalamus-pituitary-adrenal axis, secreted short-chain fatty acids, and neurotransmitter metabolism.

A comprehensive literature search was conducted using databases such as PubMed to identify studies exploring the relationship between gut microbiota and hypertension, along with the effects of dietary interventions and probiotics on blood pressure regulation.

Studies in both animal models and human subjects have demonstrated a strong correlation between alterations in gut microbiota composition and the development of hypertension. By influencing blood pressure, the gut microbiota can potentially affect the progression of cardiovascular and kidney disorders. Modulating gut microbiota through dietary interventions and probiotics has shown promise in regulating blood pressure and reducing systemic inflammation, offering a novel approach to managing hypertension. Diets such as the Mediterranean diet, which is rich in polyphenols and omega-3 fatty acids and low in sodium, promote the growth of beneficial gut bacteria that support cardiovascular health. Additionally, probiotics have been found to enhance gut barrier function, reduce inflammation, and modulate the Renin-Angiotensin System, all of which contribute to lowering blood pressure.

Further research is needed to determine the mechanisms of action of the microbiota in hypertension. The aim of this study was to evaluate the influence of gut microbiota on blood pressure regulation and the progression of hypertension-related complications, such as cardiovascular and kidney disorders.