Epigenetic modifications are heritable changes in gene expression that do not alter the DNA sequence. Histone modifications, non-coding RNA expression, and DNA methylation are examples of common epigenetic changes. Obstructive sleep apnoea-hypopnea syndrome (OSAHS) is the most common sleep-related breathing disorder, and its incidence is increasing annually, making it a hotspot of clinical research and significantly impacting health and well-being. The main cause of OSAHS is related to complications caused by repeated chronic intermittent hypoxia (CIH). Currently, polysomnography (PSG) and continuous positive airway pressure (CPAP) remain the gold standards for the diagnosis and treatment of OSAHS. However, their limitations-such as time consumption, high cost, and poor patient comfort-contribute to the paradox of high disease prevalence yet low rates of diagnosis and treatment, resulting in a substantial disease burden. In recent years, rapid advances in epigenetics have revealed that biomarkers such as microRNAs (miRNAs), circular RNAs (circRNAs), and other epigenetic modifications hold promise as non-invasive tools for the diagnosis and treatment of OSAHS and its related complications. Although numerous studies have explored epigenetic modifications in other diseases, this study focuses on how epigenetic modifications participate in the process of OSAHS and its related complications, with an aim of elucidating the pathogenesis of OSAHS from an epigenetic perspective and provide new directions for identifying molecular targets for the diagnosis and treatment of OSAHS and related complications.

Intermittent hypoxia (IH), a defining feature of obstructive sleep apnea (OSA), is associated with heart damage and linked to transient receptor potential canonical channel 5 (TRPC5). Nonetheless, the function of TRPC5 in OSA-induced cardiac injury remains uncertain. For this research, we aimed to explore the role and potential mechanism of TRPC5 in cardiomyocyte injury induced by intermittent hypoxia.

30 patients with newly diagnosed OSA and 30 patients with primary snoring(PS) were included in this study. Participants were subjected to polysomnography (PSG) for OSA diagnosis. Echocardiography was used to evaluate the structure and function of the heart, while peripheral blood samples were obtained. Additionally, RT-qPCR was utilized to quantify the relative expression level of TRPC5 mRNA in peripheral blood. H9c2 cells experienced IH or normoxia. TRPC5 levels in H9c2 cells were determined via RT-qPCR and Western blotting (WB) methods. H9c2 cells overexpressing TRPC5 were subjected to either normoxic or intermittent hypoxia conditions. Cell viability was determined by CCK8, the apoptosis rate, reactive oxygen species(ROS) levels, and Ca2+ concentration were assessed by flow cytometry, and the protein levels of TRPC5, Bcl-2, Bax, and Caspase-3 were analyzed by WB. Mitochondrial membrane potential(MMP), mitochondrial membrane permeability transition pore(mPTP), and transmission electron microscopy(TEM) were employed to observe mitochondrial function and structure. After inhibiting ROS with N-acetylcysteine (NAC), apoptosis, mitochondrial function and structure, and the concentration of Ca2+ were further detected.

TRPC5 and left atrial diameter (LAD) were higher in OSA individuals, while the E/A ratio was lower(all P<0.05). IH impaired cell viability, triggered cell apoptosis, and enhanced TRPC5 expression in H9c2 cells(all P<0.05). The effects of IH on apoptosis, cell viability, mitochondrial function and structure damage, and oxidative stress (OxS) in H9c2 cells were accelerated by the overexpression of TRPC5(all P<0.05). Furthermore, cell apoptosis and mitochondrial structural and functional damage caused by overexpression of TRPC5 were attenuated by ROS inhibition.

TRPC5 is associated with structural and functional cardiac damage in patients with OSA, and TRPC5 promotes IH-induced apoptosis and mitochondrial damage in cardiomyocytes through OxS. TRPC5 may be a novel target for the diagnosis and treatment of OSA-induced myocardial injury.

Obstructive sleep apnoea hypoventilation syndrome (OSAHS) is a common sleep disorder that affects multiple body systems, which in turn is closely associated with cognitive dysfunction, diabetes mellitus, oncological cardiovascular diseases and metabolic disorders. In recent years, non-coding RNA (ncRNA) has emerged as a new opportunity for biomarker discovery. We therefore discuss the research progress and potential role of ncRNAs in obstructive sleep apnea hypoventilation syndrome.

This review systematically searched relevant academic literature from PubMed, Web of Science and other databases. During the retrieval process, a combination of keywords such as "OSAHS", "ncRNA", "lncRNA", "miRAN", "circRNA" was used for search.

Circulating ncRNA has good area under the ROC curve, sensitivity and specificity in the diagnosis of OSAHS, and has the potential to become a diagnostic marker for OSAHS, while several circulating ncRNAs or circulating ncRNAs in combination with other tests such as the Obstructive Sleep Apnoea Screening Scale have a higher value of application as a test for OSAHS. Further analyses revealed that many circulating ncRNAs were significantly differentially expressed in the serum of OSAHS patients with different very severities, a potential marker for predicting the severity of OSAHS, and that the ncRNA content of patients' serum also had a significant effect during CPAP therapy, suggesting that it may have potential for therapeutic monitoring. Meanwhile, serum ncRNAs from patients have been shown to be effective in the diagnosis of OSAHS complications such as hypertension, Alzheimer's disease, acute myocardial infarction and atherosclerosis. The expression of up- or down-regulated ncRNAs can regulate different signalling pathways, which in turn affects various OSAHS complications such as pulmonary hypertension, diabetes mellitus, and cognitive dysfunction, and is expected to become a new direction for the treatment of these complications.

The changes in ncRNA expression in OSAHS patients are expected to be a novel biomarker for the diagnosis and treatment of OSAHS, and can also be used as a potential biomarker for the combination of diabetes mellitus, cardiovascular disease, respiratory disease, and cognitive dysfunction in OSAHS. It is believed that the continuous progress of ncRNA-related research is expected to promote the early detection, diagnosis and treatment of OSAHS and its complications.

Obstructive sleep apnea (OSA) is characterized by intermittent hypoxia (IH) and is strongly associated with adverse cardiovascular outcomes. Myocardial injury and dysfunction have been commonly observed in clinical practice, particularly in patients with severe OSA. However, the underlying mechanisms remain obscure. In this review, we summarized the molecular mechanisms by which IH impact on myocardial injury and dysfunction. In brief, IH-induced cardiomyocyte death proceeds through the regulation of multiple biological processes, including differentially expressed transcription factors, alternative epigenetic programs, and altered post-translational modification. Besides cell death, various cardiomyocyte injuries, such as endoplasmic reticulum stress, occurs with IH. In addition to the direct effects on cardiomyocytes, IH has been found to deteriorate myocardial blood and energy supply by affecting the microvascular structure and disrupting glucose and lipid metabolism. For better diagnosis and treatment of OSA, further studies on the molecular mechanisms of IH-induced myocardial injury and dysfunction are essential.

In this narrative review, we present a comprehensive assessment on the putative roles of long non-coding RNAs (lncRNAs) in intermittent hypoxia (IH) and sleep apnea. Collectively, the evidence from cell culture, animal, and clinical research studies points to the functional involvement of lncRNAs in the pathogenesis, diagnosis, and potential treatment strategies for this highly prevalent disorder. Further research is clearly warranted to uncover the mechanistic pathways and to exploit the therapeutic potential of lncRNAs, thereby improving the management and outcomes of patients suffering from sleep apnea.

Obstructive sleep apnoea (OSA) is a global health problem with important cardiovascular consequences. Risk assessment tools are essential in OSA to identify patients at increased risk of cardiovascular disease and to achieve a cost-effective clinical management of the disease in the era of precision medicine. The objective is to provide an updated perspective on the role of microRNAs (miRNAs) in OSA as a biomarker of cardiovascular risk.

Specific miRNAs have already been associated with patients with OSA and specific cardiovascular diseases such as hypertension, myocardial infarction or endothelial dysfunction. Numerous studies have addressed the use of miRNAs to identify the cardiovascular risk associated with OSA, both in patients and in animals with in vivo hypoxia models. Thus, these studies identified profiles of differentially expressed miRNAs in patients with OSA. In addition, the in vitro studies suggest that therapies with miRNA inhibitors that could help reduce cardiovascular risk. Therefore, this review highlights the primary approaches of the potential of miRNAs as biomarkers at the prognostic, diagnostic and therapeutic strategy levels.

Given the heterogeneity of OSA and its cardiovascular consequences, miRNAs have emerged as powerful biomarkers that can help improve the clinical management of OSA and its cardiovascular risk.

A growing amount of information about the different types, functions, and roles played by non-coding RNAs (ncRNAs) is becoming available, as more and more research is done. ncRNAs have been identified as potential therapeutic targets in the treatment of tuberculosis (TB), because they may be essential regulators of the gene network. ncRNA profiling and sequencing has recently revealed significant dysregulation in tuberculosis, primarily due to aberrant processes of ncRNA synthesis, including amplification, deletion, improper epigenetic regulation, or abnormal transcription. Despite the fact that ncRNAs may have a role in TB characteristics, the detailed mechanisms behind these occurrences are still unknown. The dark matter of the genome can only be explored through the development of cutting-edge bioinformatics and molecular technologies. In this review, ncRNAs' synthesis and functions are discussed in detail, with an emphasis on the potential role of ncRNAs in tuberculosis. We also focus on current platforms, experimental strategies, and computational analyses to explore ncRNAs in TB. Finally, a viewpoint is presented on the key challenges and novel techniques for the future and for a wide-ranging therapeutic application of ncRNAs.