Exosomes are small extracellular vesicles produced by most cell types and contain proteins, lipids, and nucleic acids (non-coding RNAs, mRNA, and DNA) that can be released by donor cells to influence the function of recipient cells. Skin photoaging is the premature aging of skin structures caused by prolonged exposure to ultraviolet (UV), as demonstrated by depigmentation, roughness, rhytides, elastosis, and precancerous alterations. Exosomes are associated with aging processes such as oxidative damage, inflammation, and senescence. Exosomes' anti-aging properties have been linked to various in vitro and preclinical investigations. There are still several unanswered questions about the use of MSC exosomes for skin rejuvenation, despite encouraging results. Uncertainty surrounds the precise processes by which exosomes stimulate the creation of collagen, skin tissue via a variety of mechanisms, including reduced matrix metalloproteinase (MMP) expression, increased collagen and elastin production, and modulation of intracellular signaling pathways and intercellular communication. These findings suggest the therapeutic potential of exosomes in skin aging. This review provides information on the molecular mechanisms and consequences of exosome anti-aging.

Wound healing presents a significant challenge in healthcare, imposing substantial physiological and economic burdens. While traditional treatments and stem cell therapies have shown benefits, milk-derived exosomes (MDEs) offer distinct advantages as a cell-free therapeutic approach. MDEs, isolated from mammalian milk, are characterized by their biocompatibility, ease of acquisition, and high yield, making them a promising tool for enhancing wound repair. This review provides a comprehensive analysis of the composition, sources, and extraction methods of MDEs, with a focus on their therapeutic role in both acute and diabetic chronic wounds. MDEs facilitate wound healing through the delivery of bioactive molecules, modulating key processes such as inflammation, angiogenesis, and collagen synthesis. Their ability to regulate complex wound-healing pathways underscores their potential for widespread clinical application. This review highlights the importance of MDEs in advancing wound management and proposes strategies to optimize their use in regenerative medicine.

The authors carried out a comprehensive review of the application of peptides known as cell-penetrating peptides (CPPs) in various drug delivery systems (DDS), with the prospect of achieving novel solutions and ideas to overcome the challenges of DDS, by making them more able to penetrate cells and biological membranes. A conceptual search was conducted in relevant literature databases (Scopus, PubMed, Web of Science, and Google Scholar) up to 1 April 2025 using keywords such as drug delivery systems, cell-penetrating peptides, CPPs, complexes, conjugates, nanoparticles, dendrimers, exosomes, liquid crystalline, liposomes, micelles, nanospheres and lipid nanoparticles. The studies demonstrate that the antimicrobial effect of drugs, including curcumin, gentamicin, and antifungal drugs like imidazoacridinone derivatives, can be enhanced when they are conjugated or complexed with CPPs. CPPs possess positive charges, which make them suitable for gene therapy applications by facilitating the delivery of plasmids and siRNAs with negative charges in modern delivery systems. Medicinal formulations containing CPPs in combination with liquid crystals or nanostructured lipid carriers (NLCs) increase drugs penetration to the skin. Additionally, several investigations showed that CPPs could have a positive impact on the pharmacokinetic and pharmacodynamic of chemotherapy agents, reducing their side effects. CPPs have significant potential in enhancing penetration, bioavailability, targeting, and optimization of DDS. By using computer modeling and designing CPPs with more desirable features and conducting more clinical studies, new methods for treating diseases and better formulations can be achieved.

Small extracellular vesicles (sEV) derived from mesenchymal stem cells hold promise for anti-skin aging, yet their clinical application is hindered by poor transdermal permeability. Herein, we report an innovative light-controlled sEV-based spherical nucleic acid nanomotor (NM-ESNA). This nanosystem was composed of an sEV core and an MMP1-targeting siRNA shell, forming a 3D penetrative nanostructure. In addition, asymmetrically modified light-responsive gas-generating molecules were integrated into the nanomotor, enabling efficient dermal delivery. The light-controlled and enhanced transdermal delivery guaranteed synergistic anti-skin aging therapy through sEV-mediated paracrine effects and gene therapy targeting MMP1 in the dermis. On the basis of this deep transdermal delivery technology and the synergistic therapy strategy, NM-ESNA demonstrated outstanding anti-skin aging effects in a mouse model. This biocompatible nanosystem (NM-ESNA) enabled light-controlled and deep transdermal delivery, establishing a therapeutic platform with significant potential for sEV-based noninvasive anti-skin aging therapy.

Extracellular vesicles (EVs) are membrane-bound structures released by cells carrying diverse biomolecules involved in intercellular communication. Small EVs are abundant in body fluids, playing a key role in cell signaling. Their natural occurrence and therapeutic potential, especially in the context of muscular disorders, make them a significant area of research. Sarcopenia, characterized by progressive muscle fiber loss, represents a pathological state in which EVs could offer therapeutic benefits, reducing morbidity and mortality. Recent studies have proposed an interplay between adipose tissue (AT) and skeletal muscle regarding sarcopenia pathology. AT dysregulation, as seen in obesity, contributes to skeletal muscle loss in a multifactorial way. While AT-derived stem cell (ATDSC) small EVs have been implicated in musculoskeletal homeostasis, their precise action in muscle regeneration remains incompletely understood. In this context, ATDSC-derived small EVs can stimulate skeletal muscle regeneration through improved proliferation and migration of muscle cells, enhancement of muscular perfusion, improvement of tendon and nerve regeneration, stimulation of angiogenesis, and promotion of myogenic differentiation. However, they can also increase skeletal muscle loss. Notably, this is the first comprehensive review to systematically examine the role of ATDSC-derived small EVs in sarcopenia.

Asthma is a complex, multifactorial inflammatory disorder of the airways, characterized by recurrent symptoms and variable airflow obstruction. So far, two main asthma endotypes have been identified, type 2 (T2)-high or T2-low, based on the underlying immunological mechanisms. Recently, extracellular vesicles (EVs), particularly exosomes, have gained increasing attention due to their pivotal role in intercellular communication and distal signaling modulation. In the context of asthma pathobiology, an increasing amount of experimental evidence suggests that EVs secreted by eosinophils, mast cells, dendritic cells, T cells, neutrophils, macrophages, and epithelial cells contribute to disease modulation. This review explores the role of EVs in profiling the molecular signatures of T2-high and T2-low asthma, offering novel perspectives on disease mechanisms and potential therapeutic targets.

Nonsurgical facial esthetic procedures have revolutionized cosmetic enhancement, offering minimally invasive options for facial rejuvenation. This comprehensive overview covers a wide range of techniques, including wrinkle relaxation with botulinum toxin, skin volumization using dermal fillers and biostimulators, hair restoration, and various skin tightening and texture improvement methods. The article details the mechanisms, applications, and potential risks of each procedure, highlighting recent advancements and trends in the field. It classifies these treatments into clinically-oriented categories based on patients' desired changes.

Exosomes, nanosized extracellular vesicles released by various cell types, are intensively studied for the diagnosis and treatment of cancer and neurodegenerative diseases, and they also display high usability in regenerative medicine. Emphasizing their diagnostic potential, exosomes serve as carriers of disease-specific biomarkers, enabling non-invasive early detection and personalized medicine. The cargo loading of exosomes with therapeutic agents presents an innovative strategy for targeted drug delivery, minimizing off-target effects and optimizing therapeutic interventions. In regenerative medicine, exosomes play a crucial role in intercellular communication, facilitating tissue regeneration through the transmission of bioactive molecules. While acknowledging existing challenges in standardization and scalability, ongoing research efforts aim to refine methodologies and address regulatory considerations. In summary, this review underscores the transformative potential of exosomes in reshaping the landscape of medical interventions, with a particular emphasis on cancer, neurodegenerative diseases, and regenerative medicine.

Cancer continues to be a prominent fatal health issue worldwide, driving the urgent need for more effective treatment strategies. The pressing demand has sparked significant interest in the development of advanced drug delivery systems for chemotherapeutics. The advent of nanotechnology offers a groundbreaking approach, presenting a promising pathway to revolutionize cancer treatment and improve patient outcomes. Nanomedicine-based drug delivery systems have demonstrated the capability of improving the pharmacokinetic properties and accumulation of chemotherapeutic agents in cancer sites while minimizing the adverse side effects. Despite these advantages, most NDDSs exhibit only limited improvement in cancer treatment during clinical trials. The recent development of magnetic nanoparticles (MNPs) for biomedical applications has revealed a potential opportunity to further enhance the performance of NDDSs. The magnetic properties of MNPs can be utilized to increase the targeting capabilities of NDDSs, improve the controlled release of chemotherapeutic agents, and weaken the chemoresistance of tumors with magnetic hyperthermia. In this review, we will explore recent advancements in research for NDDSs for oncology applications, how MNPs and their properties can augment the capabilities of NDDSs when complexed with them and emphasize the challenges and safety concerns of incorporating these systems into cancer treatment.

Acute lung injury being one of the earliest and most severe complications during sepsis and macrophages play a key role in this process. To investigate the regulatory effects and potential mechanisms of adipose mesenchymal stem cell derived-exosomes (ADSC-exo) on macrophages and septic mice, ADSCs-exo was administrated to both LPS-induced macrophage and cecal ligation and puncture (CLP) induced sepsis mice. ADSCs-exo was confirmed to inhibit M1 polarization of macrophages and to reduce excessive inflammation. The use of ADSCs-exo in CLP mice and in LPS-induced macrophages relieved oxidative stress, cellular damage, and acute lung injury. During this process, ADSCs-exo increased the nuclear translocation of Nrf2, significantly upregulating the activation of the antioxidant pathway Nrf2/HO-1. Concurrently, they enhanced the expression of SIRT1 in macrophages. Further SIRT1 interference experiments demonstrated that ADSCs-exo mitigated macrophage inflammatory responses and LPS-induced ferroptosis by upregulating SIRT1. In the LPS-induced macrophage model, after SIRT1 was interfered with, ADSCs-exo failed to upregulate the Nrf2/HO-1 signaling pathway, leading to enhanced ferroptosis. Finally, in a CLP sepsis mouse model with myeloid-specific SIRT1 knockout, ADSCs-exo was observed to reduce lung tissue injury, oxidative stress damage, and ferroptosis. Still, these beneficial effects were reversed due to the myeloid-specific knockout of SIRT1, while co-administration of a ferroptosis inhibitor rescued this situation, alleviating lung injury and significantly reducing tissue levels of oxidative stress. In conclusion, this study elucidated a novel potential therapeutic mechanism wherein ADSCs-exo upregulates the levels of SIRT1 in macrophages through a non-delivery approach.

Endometrial injury caused by repeated uterine procedures, infections, inflammation, or uterine artery dysfunction can deplete endometrial stem/progenitor cells and impair regeneration, thereby diminishing endometrial receptivity and evidently lowering the live birth, clinical pregnancy, and embryo implantation rates. Currently, safe and effective clinical treatment methods or gene-targeted therapies are unavailable, especially for severe endometrial injury. Umbilical cord mesenchymal stem cells and their extracellular vesicles are characterized by their simple collection, rapid proliferation, low immunogenicity, and tumorigenicity, along with their involvement in regulating angiogenesis, immune response, cell apoptosis and proliferation, inflammatory response, and fibrosis, Therefore, these cells and vesicles hold broad potential for application in endometrial repair. This article reviewed recent research on human umbilical cord mesenchymal stem cells as well as their extracellular vesicles in repairing endometrial injury.

The skin functions as the body's primary defense barrier; when compromised, it can lead to dehydration, infection, shock, or potentially life-threatening conditions. Miniature pigs exhibit skin characteristics and healing processes highly analogous to humans. Mesenchymal stem cells contribute to skin injury repair through a paracrine mechanism involving exosomes. This research examines whether adipose-derived MSC exosomes effectively enhance healing following autologous skin grafting in miniature pigs. It also compares the roles and distinctions of ADSCs and ADSC-Exos in inflammatory responses and tissue regeneration. This study found significantly reduced levels of oxidative stress products and pro-inflammatory factors, while antioxidant factors, anti-inflammatory factors, and pro-regenerative factors were elevated, and anti-regenerative factor levels decreased. Moreover, the expression levels of key markers-namely, PI3K, Akt, and mTOR-in the regeneration-associated signaling pathway were increased. The alterations in these indicators indicate that ADSC-Exos can regulate inflammatory responses and promote regeneration. This study provides a novel theoretical foundation for the implementation of acellular therapy in clinical settings.

Extracellular vesicles have emerged as promising nanocarriers for targeted drug delivery, but their therapeutic potential is limited by challenges related to administration route, loading, targeted delivery and production at scale. Here, we report an innovative approach for targeted delivery of therapeutic peptides to injured tissues using milk-derived small extracellular vesicles (mEVs) as an abundant, safe, orally administrable nanoplatform. We demonstrate that a sub-population of mEVs naturally contain Connexin 43 (Cx43) and its Carboxyl-Terminal (CT) polypeptides, which have been shown to play crucial roles in wound healing and tissue repair. Leveraging this intrinsic property, we developed an esterification method to efficiently and uniformly load mEVs with enhanced levels of an exogenous Cx43 CT peptide (αCT11 - RPRPDDLEI), as assessed by flow cytometry-based vesicle quantification and mass spectrometry. These engineered mEVs exhibited remarkable injury targeting capabilities, with > 30-fold increases in uptake by injured cells compared to non-wounded cells in vitro and preferential accumulation in wounded tissues in vivo. Notably, αCT11-loaded mEVs orally administered after myocardial infarction reduced infarct size by >60% and preserved heart function in a mouse model of ischemia-reperfusion injury. This study represents a significant advance in nanomedicine, demonstrating the utilization of naturally occurring milk-derived extracellular vesicles as an oral delivery system for therapeutic peptides, achieving unprecedented targeting efficiency and efficacy in the treatment of myocardial ischemia-reperfusion injury.

Exosomes (Exos) from adipose derived stem cells (ADSCs) can delay skin photoaging, but their effects on reactive oxygen species (ROS) remains unclear. This study aimed to investigate the relationship between adipose derived stem cell exosomes (ADSCs-Exos) in anti-photoaging of skin and glutathione (GSH)/ ROS expression in human fibroblasts.

A skin photoaging model was established by irradiating human fibroblasts with ultraviolet B (UVB) light in vitro. Next, exosomes from ADSCs were isolated for treating the photoaged fibroblasts. Afterwards, the alterations in photoaged fibroblasts were analyzed by a series of assays including senescence-associated β-galactosidase (SA-β-Gal) staining, p16 expression, ROS staining, and GSH content.

After a human fibroblast photoaging model was subjected to ADSCs-Exos treatment, we found that the high concentration exosome group had the highest GSH content. Cellular staining showed that levels of SA-β-Gal, p16, and ROS of the high concentration-treated group were lower than other groups.

ADSCs-Exos can protect skin fibroblasts from photoaging via increasing the ratio of GSH/ROS.

In the medical field, wound healing poses significant challenges due to its complexity and time-consuming nature. Cell-free wound repair, notably the utilization of exosomes (EXOs), has made significant progress in recent years. Urine, saliva, umbilical cord, blood, mesenchymal stem cells and breast milk cells can be used to extract and purify EXOs, which are Nano-sized lipid bilayer vesicles. Besides their relatively little toxicity, non-specific immunogenicity and excellent biocompatibility, EXOs also contain bioactive molecules such as proteins, lipids, microRNAs (miRNAs), and messenger RNAs (mRNAs). Their bioactive compounds have anti-inflammatory properties and can speed up wound healing. Various medicinal agents can also be contained within the EXOs. This review briefly provides new information on the different aspects of EXOs and evaluate the application of EXOs as a promising therapy in the regeneration of skin wounds in recent pre-clinical and clinical studies.

Due to overactive inflammation and hindered angiogenesis, self-healing of diabetic wounds (DW) remains challenging in the clinic. Platelet-derived exosomes (PLT-Exos), a novel exosome capable of anti-inflammation and pro-angiogenesis, show great potential in DW treatment. However, previous administration of exosomes into skin wounds is topical daub or intradermal injection, which cannot intradermally deliver PLT-Exos into the dermis layer, thus impeding its long-term efficacy in anti-inflammation and pro-angiogenesis. Herein, a dissolvable microneedle-based wound dressing (PLT-Exos@ADMMA-MN) was developed for transdermal and long-term delivery of PLT-Exos. Firstly, a photo-crosslinking methacrylated acellular dermal matrix-based hydrogel (ADMMA-GEL), showing physiochemical tailorability, fast-gelling performance, excellent biocompatibility, and pro-angiogenic capacities, was synthesized as a base material of our dressing. For endowing the dressing with anti-inflammation and pro-angiogenesis, PLT-Exos were encapsulated into ADMMA-GEL with a minimum effective concentration determined by our in-vitro experiments. Then, in-vitro results show that this dressing exhibits excellent properties in anti-inflammation and pro-angiogenesis. Lastly, in-vivo experiments showed that this dressing could continuously and transdermally deliver PLT-Exos into skin wounds to switch local macrophage into M2 phenotype while stimulating neovascularization, thus proving a low-inflammatory and pro-angiogenic microenvironment for DW healing. Collectively, this study provides a novel wound dressing capable of suppressing inflammation and stimulating vascularization for DW treatment.

The prevalence of female reproductive system disorders is increasing, especially among women of reproductive age, significantly impacting their quality of life and overall health. Managing these diseases effectively is challenging due to the complex nature of the female reproductive system, characterized by dynamic physiological environments and intricate anatomical structures. Innovative drug delivery approaches are necessary to facilitate the precise regulation and manipulation of biological tissues. Nanotechnology is increasingly considered to manage reproductive system disorders, for example, nanomaterial imaging allows for early detection and enhances diagnostic precision to determine disease severity and progression. Additionally, nano drug delivery systems are gaining attention for their ability to target the reproductive system successfully, thereby increasing therapeutic efficacy and decreasing side effects. This comprehensive review outlines the anatomy of the female upper genital tract by highlighting the complex mucosal barriers and their impact on systemic and local drug delivery. Advances in nano drug delivery are described for their sustainable therapeutic action and increased biocompatibility to highlight the potential of nano drug delivery strategies in managing female upper genital tract disorders.

Exosomes (Exos) are candidates for functional recovery and regeneration following sciatic nerve crushed (SNC) injury due to their composition which can accelerate tissue regeneration. Therefore, mouse embryonic fibroblast-derived exosomes were evaluated for their regenerative capacity in SNC injury.

In the study, 40 Balb/c males (20 ± 5 g) and two pregnant mice (for embryonic fibroblast tissue) were used and crushed injury was induced in the left sciatic nerve with an aneurysm clamp. Sciatic nerve model mice were randomly divided into 5 groups (n = 8; control, n = 8; sham, n = 8; SNC, n = 8; Mouse embryonic fibroblast exosome (mExo), n = 8; SNC + Mouse embryonic fibroblast exosome (SNC + mExo). Rotarod tests for motor functions and hot plate and von Frey tests for sensory functions were analyzed in the groups. Expression changes of exosome genes (RARRES1, NAGS, HOXA13, and MEIS1) immunohistochemical analysis of these gene proteins, and structural exosome NF-200 and S100 proteins were evaluated by confocal microscopy. Behavioral analyses showed that the damage in SNC was significant between groups on day14 and day28 (P < 0.05). In behavioral analyses, it was determined that motor functions and mechanical sensitivity lost in SNC were regained after mExo treatment. While expression of all genes was detected in MEF-derived exosomes, the high expression was MESI1 and the low expression was HOXA13. NF200, an indicator of axon number and neurofilament density, was found to decrease in SNC (P < 0.001) and increase after treatment, but not significantly. The decreased S100 protein levels in SNC and the increase detected after treatment were not significant.

The expression of four mRNAs in mExos indicates that these genes may have an effect on regenerative processes after SNC injury. The regenerative process supported by tissue protein expressions demonstrates the therapeutic potential of mExo treatment.

Exosomes exhibit high bioavailability, biological stability, targeted specificity, low toxicity, and low immunogenicity in shuttling various bioactive molecules such as proteins, lipids, RNA, and DNA. Natural exosomes, however, have limited production, targeting abilities, and therapeutic efficacy in clinical trials. On the other hand, engineered exosomes have demonstrated long-term circulation, high stability, targeted delivery, and efficient intracellular drug release, garnering significant attention. The engineered exosomes bring new insights into developing next-generation drug delivery systems and show enormous potential in therapeutic applications, such as tumor therapies, diabetes management, cardiovascular disease, and tissue regeneration and repair. In this review, we provide an overview of recent advancements associated with engineered exosomes by focusing on the state-of-the-art strategies for cell engineering and exosome engineering. Exosome isolation methods, including traditional and emerging approaches, are systematically compared along with advancements in characterization methods. Current challenges and future opportunities are further discussed in terms of the preparation and application of engineered exosomes.

The skin plays a crucial role as a protective barrier against external factors, but disruptions to its integrity can lead to wound formation and hinder the natural healing process. Scar formation and delayed wound healing present significant challenges in skin injury treatment. While alternative approaches such as skin substitutes and tissue engineering exist, they are often limited in accessibility and cost. Exosomes have emerged as a potential solution for wound healing due to their regenerative properties.

In this study, exosomes were isolated from human blood serum using a kit. The exosomes were characterized, and their effects on cell migration were assessed in vitro. Additionally, the wound healing capacity of exosomes was evaluated in vivo using a rat full-thickness wound model.

Our in vitro findings revealed that exosomes significantly promoted cell migration. In vivo experiments demonstrated that the injection of exosomes at different areas of the wound accelerated the wound healing process, resulting in wound closure, collagen synthesis, vessel formation, and angiogenesis in the wound area. These results suggest that exosomes have a promising therapeutic potential for expediting wound healing and minimizing scar formation.

The findings of this study highlight the potential of exosomes as a novel approach for enhancing wound healing. Exosomes showed positive effects on both cell migration and wound closure in in vitro and in vivo studies, suggesting their potential use as a regenerative therapy for skin injuries. Further research is needed to fully understand the mechanisms underlying the beneficial effects of exosomes on wound healing and to optimize their application in clinical settings.

Recent studies have emphasized the critical role of Telocytes (TCs)-derived exosomes in organ tissue injury and repair. Our previous research showed a significant increase in ITGB1 within TCs. Pulmonary Arterial Hypertension (PAH) is marked by a loss of microvessel regeneration and progressive vascular remodeling. This study aims to investigate whether exosomes derived from ITGB1-modified TCs (ITGB1-Exo) could mitigate PAH.

We analyzed differentially expressed microRNAs (DEmiRs) in TCs using Affymetrix Genechip miRNA 4.0 arrays. Exosomes isolated from TC culture supernatants were verified through transmission electron microscopy and Nanoparticle Tracking Analysis. The impact of miR-429-3p-enriched exosomes (Exo-ITGB1) on hypoxia-induced pulmonary arterial smooth muscle cells (PASMCs) was evaluated using CCK-8, transwell assay, and inflammatory factor analysis. A four-week hypoxia-induced mouse model of PAH was constructed, and H&E staining, along with Immunofluorescence staining, were employed to assess PAH progression.

Forty-five miRNAs exhibited significant differential expression in TCs following ITGB1 knockdown. Mus-miR-429-3p, significantly upregulated in ITGB1-overexpressing TCs and in ITGB1-modified TC-derived exosomes, was selected for further investigation. Exo-ITGB1 notably inhibited the migration, proliferation, and inflammation of PASMCs by targeting Rac1. Overexpressing Rac1 partly counteracted Exo-ITGB1's effects. In vivo administration of Exo-ITGB1 effectively reduced pulmonary vascular remodeling and inflammation.

Our findings reveal that ITGB1-modified TC-derived exosomes exert anti-inflammatory effects and reverse vascular remodeling through the miR-429-3p/Rac1 axis. This provides potential therapeutic strategies for PAH treatment.

This study investigates the intricate interplay between environmental pollutants and exosomes, shedding light on a novel paradigm in environmental health and disease. Cellular stress, induced by environmental toxicants or disease, significantly impacts the production and composition of exosomes, crucial mediators of intercellular communication. The heat shock response (HSR) and unfolded protein response (UPR) pathways, activated during cellular stress, profoundly influence exosome generation, cargo sorting, and function, shaping intercellular communication and stress responses. Environmental pollutants, particularly lipophilic ones, directly interact with exosome lipid bilayers, potentially affecting membrane stability, release, and cellular uptake. The study reveals that exposure to environmental contaminants induces significant changes in exosomal proteins, miRNAs, and lipids, impacting cellular function and health. Understanding the impact of environmental pollutants on exosomal cargo holds promise for biomarkers of exposure, enabling non-invasive sample collection and real-time insights into ongoing cellular responses. This research explores the potential of exosomal biomarkers for early detection of health effects, assessing treatment efficacy, and population-wide screening. Overcoming challenges requires advanced isolation techniques, standardized protocols, and machine learning for data analysis. Integration with omics technologies enhances comprehensive molecular analysis, offering a holistic understanding of the complex regulatory network influenced by environmental pollutants. The study underscores the capability of exosomes in circulation as promising biomarkers for assessing environmental exposure and systemic health effects, contributing to advancements in environmental health research and disease prevention.

Previous studies have demonstrated a significant upregulation of Integrin Beta 1 (ITGB1) in Telocytes. This study aims to explore the roles and underlying mechanisms of ITGB1 in inflammation and oxidative stress following Lipo-polysaccharide (LPS) administration in Telocytes.

We observed an increase in reactive oxygen species (ROS) production, accompanied by a reduction in ITGB1 levels post-LPS treatment.

Notably, inhibiting ROS synthesis markedly reduced LPS-induced ITGB1 expression. Additionally, ectopic ITGB1 expression mitigated LPS-induced inflammation and oxidative stress, evident through decreased levels of pro-inflammatory markers such as Tumor Necrosis Factor-alpha (TNF-α), Interleukin (IL)-1β, IL-6, and Monocyte Chemoattractant Protein (MCP)-1. Depletion of endothelial Yes-Associated Protein 1 (YAP1) notably diminished the levels of inflammatory markers and ROS production. Furthermore, exosomes secreted by ITGB1-modified Telocytes promoted Human Umbilical Vein Endothelial Cells (HUVECs) proliferation and inhibited apoptosis. In vivo experiments revealed that exosomes from ITGB1-modified Telocytes modulated functional and structural changes, as well as inflammatory responses in Acute Lung Injury (ALI).

These findings highlight the critical role of the YAP1/ROS axis in LPS-induced Telocyte injuries, underlining the therapeutic potential of targeting ITGB1 for mitigating inflammation and oxidative stress in these cells.

In this narrative review, we sought to provide a comprehensive overview of the mechanisms underlying cutaneous senescence, framed by the twelve traditional hallmarks of aging. These include genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, impaired macroautophagy, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, chronic inflammation, and dysbiosis. We also examined how topical interventions targeting these hallmarks can be integrated with conventional aesthetic medicine techniques to enhance skin rejuvenation. The potential of combining targeted topical therapies against the aging hallmarks with minimally invasive procedures represents a significant advancement in aesthetic medicine, offering personalized and effective strategies to combat skin aging. The reviewed evidence paves the way for future advancements and underscores the transformative potential of integrating scientifically validated interventions targeted against aging hallmarks into traditional aesthetic practices.

Our previous study showed that miR-146a-3p was elevated in serum exosomes of allergic rhinitis (AR) patients, but the underlying mechanisms were unclarified. This study was to investigate the impact of exosome-derived miR-146a-3p on macrophage polarization in the pathology of AR.

We detected the expression of miR-146a-3p in nasal tissues of AR patients and healthy controls (HCs), and investigated its correlation with macrophage polarization markers. The impact of miR-146a-3p derived from AR serum exosomes on macrophage polarization was examined. Transcriptome sequencing was performed on macrophages treated with a miR-146a-3p inhibitor, and target genes of miR-146a-3p were explored through a combination of bioinformatics analysis and experimental validation.

The expressions of miR-146a-3p and macrophage polarization markers were increased in the AR nasal tissues, and a positive association was observed between the expressions of miR-146a-3p and the levels of CD163 and CD206. The AR serum exosomes could be uptake by macrophages, and promote M2 polarization and cytokine secretions. Mechanistically, miR-146a-3p regulation could impact both macrophage M2 polarization and cytokine secretion. Inhibition of miR-146a-3p altered the gene transcriptions within macrophages. Bioinformatics analysis and clinical pathological specimen research confirmed that VAV3 was a target gene of miR-146a-3p, and it exerted a detrimental effect on macrophage M2 polarization via the PI3K/AKT/mTOR pathway. Functional recovery experiments and dual-luciferase reporter gene assays confirmed that miR-146a-3p could selectively target and inhibit the expression of VAV3, thereby promoting macrophage M2 polarization through the PI3K/AKT/mTOR pathway.

Serum exosome-derived miR-146a-3p facilitated macrophage M2 polarization in AR by targeting VAV3 through the PI3K/AKT/mTOR pathway. These findings implied that miR-146a-3p and VAV3 could serve as potential targets for the development of novel therapeutic strategies in AR management.