---
title: "Extracellular vesicles in senescence-associated chronic lung diseases"
id: "pubmed-42438973"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42438973"
content_type: "clinical_feed_article"
specialty: "Critical Care"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42438973/"
doi: "10.1097/CM9.0000000000004208"
published_at: "2026-08-20T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Extracellular vesicles in senescence-associated chronic lung diseases
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42438973
- **Specialty:** [Critical Care](https://medichelpline.com/clinical-feed/critical-care.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42438973/)
- **DOI:** [10.1097/CM9.0000000000004208](https://doi.org/10.1097%2FCM9.0000000000004208)
- **Published At:** 2026-08-20T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- Chronic lung diseases (COPD, IPF, asthma, obstructive sleep apnea, bronchiectasis, lung cancer) are closely linked to aging and cellular senescence. - **Extracellular vesicles (EVs)** produced by senescent cells mediate intercellular communication and carry cargo such as microRNAs, proteins, nucleic acids, and lipids that influence neighboring cells. - EV subtypes include **exosomes (30–100 nm)**, **microvesicles (100–1000 nm)**, and **apoptotic bodies (500 nm–5 μm)**, originating from multivesicular bodies, the plasma membrane, or apoptotic cells. - EV cargo implicated in lung disease progression includes microRNAs (notably **miR-21**, **miR-34a**, **miR-570-3p**) and multiple proteins that promote inflammation, fibrosis, tissue remodeling, and propagation of senescence. - Senescent cells exhibit markers such as increased SA-β-gal activity, elevated **p16** and **p21**, and heightened ROS; they secrete a senescence-associated secretory phenotype (SASP) that includes EVs. - Key lung cell types releasing pathogenic EVs are airway and alveolar epithelial cells, fibroblasts, macrophages, neutrophils, and endothelial cells; EVs can induce telomere shortening, DNA damage, oxidative stress, and cell-cycle arrest in recipient cells. - EVs modulate immune responses and can have both proinflammatory and potential anti-inflammatory effects; their roles in immune regulation offer therapeutic opportunities. - Experimental uses of EVs include therapeutic agents and nanotechnology-based targeted delivery to reduce inflammation, modulate immunity, and support tissue repair, but clinical safety and efficacy remain to be validated. - Important gaps include limited exploration of EV component effects across cell types, need for standardized EV isolation and characterization methods, and rigorous clinical trials to verify EV-based therapies. - Understanding EV biology in aging-related lung disease could identify therapeutic targets to slow disease progression and improve outcomes; further mechanistic work is required.
## Clinical Analysis & Structured Key Points
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Epub 2026 Jul 13. # Extracellular vesicles in senescence-associated chronic lung diseases [Ruiying Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+R&cauthor_id=42438973)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42438973/#full-view-affiliation-1 "Department of Pulmonary and Critical Care Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, Shanxi 030032, China."), [Yahong Chen](https://pubmed.ncbi.nlm.nih.gov/?term=Chen+Y&cauthor_id=42438973)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42438973/#full-view-affiliation-2 "Department of Pulmonary and Critical Care Medicine, Peking University Third Hospital, Beijing 100191, China."), [Xiansheng Liu](https://pubmed.ncbi.nlm.nih.gov/?term=Liu+X&cauthor_id=42438973)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42438973/#full-view-affiliation-1 "Department of Pulmonary and Critical Care Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, Shanxi 030032, China.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42438973/#full-view-affiliation-3 "Department of Pulmonary and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China."), [Peter J Barnes](https://pubmed.ncbi.nlm.nih.gov/?term=Barnes+PJ&cauthor_id=42438973)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42438973/#full-view-affiliation-4 "National Heart and Lung Institute, Imperial College, London SW3 6LY, United Kingdom.") Affiliations Expand ### Affiliations * 1 Department of Pulmonary and Critical Care Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, Shanxi 030032, China. * 2 Department of Pulmonary and Critical Care Medicine, Peking University Third Hospital, Beijing 100191, China. * 3 Department of Pulmonary and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China. * 4 National Heart and Lung Institute, Imperial College, London SW3 6LY, United Kingdom. * PMID: **42438973** * PMCID: [ PMC13485837 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13485837/) * DOI: [ 10.1097/CM9.0000000000004208 ](https://doi.org/10.1097/cm9.0000000000004208) Item in Clipboard Review # Extracellular vesicles in senescence-associated chronic lung diseases Ruiying Wang et al. Chin Med J (Engl). 2026. Show details Display options Display options Format Abstract PubMed PMID Chin Med J (Engl) Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Chin+Med+J+%28Engl%29%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Chin+Med+J+%28Engl%29%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42438973/) . 2026 Aug 20;139(16):2392-2408. doi: 10.1097/CM9.0000000000004208. Epub 2026 Jul 13. ### Authors [Ruiying Wang](https://pubmed.ncbi.nlm.nih.gov/?term=Wang+R&cauthor_id=42438973)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42438973/#short-view-affiliation-1 "Department of Pulmonary and Critical Care Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, Shanxi 030032, China."), [Yahong Chen](https://pubmed.ncbi.nlm.nih.gov/?term=Chen+Y&cauthor_id=42438973)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42438973/#short-view-affiliation-2 "Department of Pulmonary and Critical Care Medicine, Peking University Third Hospital, Beijing 100191, China."), [Xiansheng Liu](https://pubmed.ncbi.nlm.nih.gov/?term=Liu+X&cauthor_id=42438973)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42438973/#short-view-affiliation-1 "Department of Pulmonary and Critical Care Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, Shanxi 030032, China.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42438973/#short-view-affiliation-3 "Department of Pulmonary and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China."), [Peter J Barnes](https://pubmed.ncbi.nlm.nih.gov/?term=Barnes+PJ&cauthor_id=42438973)[ 4 ](https://pubmed.ncbi.nlm.nih.gov/42438973/#short-view-affiliation-4 "National Heart and Lung Institute, Imperial College, London SW3 6LY, United Kingdom.") ### Affiliations * 1 Department of Pulmonary and Critical Care Medicine, Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Tongji Shanxi Hospital, Third Hospital of Shanxi Medical University, Taiyuan, Shanxi 030032, China. * 2 Department of Pulmonary and Critical Care Medicine, Peking University Third Hospital, Beijing 100191, China. * 3 Department of Pulmonary and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030, China. * 4 National Heart and Lung Institute, Imperial College, London SW3 6LY, United Kingdom. * PMID: **42438973** * PMCID: [ PMC13485837 ](https://pmc.ncbi.nlm.nih.gov/articles/PMC13485837/) * DOI: [ 10.1097/CM9.0000000000004208 ](https://doi.org/10.1097/cm9.0000000000004208) Item in Clipboard Full text links Cite Display options Display options Format Abstract PubMed PMID ## Abstract Chronic lung diseases, such as chronic obstructive pulmonary disease, idiopathic pulmonary fibrosis, obstructive sleep apnea, asthma, bronchiectasis, and lung cancer, are intricately linked to the aging process. These diseases are characterized by a high prevalence rate and a paucity of effective treatment options. Emerging evidence highlights the critical role of extracellular vesicles (EVs) in the pathogenesis and progression of these diseases. EVs, released by senescent cells, mediate intercellular communication and modulate immune responses through their cargo of microRNAs, proteins, and other molecules. These vesicles contribute to disease progression by promoting inflammation, fibrosis, tissue remodeling, and cellular senescence. Specifically, certain microRNAs, such as miR-21, miR-34a, and miR-570-3p, along with several proteins in EVs, have been identified as key factors influencing these processes. Additionally, EVs play significant roles in immune regulation and have potential anti-inflammatory effects, making them promising candidates for therapeutic applications. Recent advances in the use of EVs as therapeutic agents, including their application in nanotechnology for targeted drug delivery, have demonstrated potential in reducing inflammation, modulating immune responses, and enhancing tissue repair. Understanding the role of EVs in these diseases offers insights into potential therapeutic targets to mitigate disease progression and improve patient outcomes. Future research should focus on standardizing EV isolation and characterization methods, verifying the safety and efficacy of EV-based therapies in clinical trials, and elucidating the complex biological mechanisms of EVs in aging and disease. **Keywords:** Asthma; Bronchiectasis; Chronic obstructive pulmonary disease (COPD); Extracellular vesicles; Idiopathic pulmonary fibrosis (IPF); Lung cancer; Obstructive sleep apnea; Senescence. Copyright © 2026 The Chinese Medical Association, produced by Wolters Kluwer Health, LLC. under the CC-BY-NC-ND license. [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement None. ## Figures [ ![Figure 1](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3160/13485837/4b32fa7caea3/cm9-139-2392-g001.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3160/13485837/a409933235ef/cm9-139-2392-g001.jpg) ** Figure 1 ** Structure and biological function of… ** Figure 1 ** Structure and biological function of extracellular vesicle (EV). The formation, structure, and disease… **Figure 1** Structure and biological function of extracellular vesicle (EV). The formation, structure, and disease associations of EVs. EVs, including exosomes (30–100 nm), microvesicles (100–1000 nm), and apoptotic bodies (500 nm–5 μm), originate from multivesicular bodies, directly from the plasma membrane, or from apoptotic cells. They carry essential cargo such as nucleic acids, proteins, and lipids. EVs are implicated in a spectrum of diseases where cellular senescence plays a significant role, such as neurodegenerative disorders, cardiovascular diseases, pulmonary conditions, renal impairments, liver diseases, gastrointestinal inflammations, dermatological conditions, ocular degenerations, and musculoskeletal disorders. Their ability to mediate communication between cells and transport pathological molecules positions EVs as key contributors to the aging process and the progression of age-associated diseases. ALS: Amyotrophic lateral sclerosis. Created with BioRender.com. [ ![Figure 2](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3160/13485837/88e947e5a56a/cm9-139-2392-g002.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3160/13485837/4c0223347457/cm9-139-2392-g002.jpg) ** Figure 2 ** This figure illustrates the involvement… ** Figure 2 ** This figure illustrates the involvement of various cell types and their secreted EVs… **Figure 2** This figure illustrates the involvement of various cell types and their secreted EVs in cellular senescence. Different cells, including airway epithelial cells, alveolar epithelial cells, fibroblasts, macrophages, neutrophils, and endothelial cells, release EVs containing specific microRNAs and other molecules. These EV contents contribute to cellular senescence by causing telomere shortening, oxidative stress, DNA damage, inflammatory signals, and cell cycle arrest. The resulting senescence leads to chronic inflammation, tissue damage, inhibited lung repair, exacerbation of lung disease, and the development of comorbidities. However, the roles of EV components in mediating biological effects across various cell types—including epithelial cells, fibroblasts, and immune cells—remain relatively underexplored. EVs: Extracellular vesicles; P16: Cyclin-dependent kinase inhibitor 2A; P21: Cyclin-dependent kinase inhibitor 1A; ROS: Reactive oxygen species; SA-β-gal: Senescence-associated β-galactosidase; SASP: Senescence-associated secretory phenotype. Created with BioRender.com. [ ![Figure 3](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3160/13485837/a0a2f51221d8/cm9-139-2392-g003.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3160/13485837/7099fce7913d/cm9-139-2392-g003.jpg) ** Figure 3 ** Cellular senescence and extracellular vesicles… ** Figure 3 ** Cellular senescence and extracellular vesicles (EVs). The role of EVs in cellular senescence… **Figure 3** Cellular senescence and extracellular vesicles (EVs). The role of EVs in cellular senescence and their impact on lung disease pathogenesis are shown. Senescence is characterized by increased SA-β-gal activity, elevated levels of cell cycle inhibitors p16 and p21, and heightened ROS production. Senescent cells secrete a SASP, which includes cytokines, chemokines, growth factors, and EVs. These EVs carry specific miRNAs, proteins, and other molecules that propagate senescence signals to surrounding cells, exacerbating tissue damage and inflammation. Key cell types involved in lung senescence include airway and alveolar epithelial cells, which serve as primary sites of senescence; fibroblasts, which contribute to tissue remodeling and fibrosis; immune cells (macrophages, neutrophils, and lymphocytes), which participate in inflammatory responses; and endothelial cells, which are involved in vascular changes. AUF-1: AU-rich element-binding factor 1; circXPO1: Circular RNA XPO1; miRNAs (miR): MicroRNAs; MMP-9: Matrix metalloproteinase-9; piRNA: Piwi-interacting RNA; ROS: Reactive oxygen species; SASP: Senescence-associated secretory phenotype. Created with BioRender.com. [ ![Figure 4](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3160/13485837/806f67fdcdc6/cm9-139-2392-g004.gif) ](https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3160/13485837/5bee1483b00c/cm9-139-2392-g004.jpg) ** Figure 4 ** EVs contribute to COPD pathogenesis… ** Figure 4 ** EVs contribute to COPD pathogenesis via fibrosis, inflammation, impaired repair, and senescence. AECs:… **Figure 4** EVs contribute to COPD pathogenesis via fibrosis, inflammation, impaired repair, and senescence. AECs: Alveolar epithelial cells; AP-1: Activator protein 1; ASMCs: Airway smooth muscle cells; CDKN1B: Cyclin-dependent kinase inhibitor 1B; COPD: Chronic obstructive pulmonary disease; CS: Cigarette smoke; ECM: Extracellular matrix; ECs: Epithelial cells; EMT: Epithelial–mesenchymal transition; EVs: Extracellular vesicles; HIF-1α: Hypoxia-inducible factor 1 alpha; IL-1β: Interleukin 1 beta; JAK/STAT: Janus kinase/signal transducer and activator of transcription; JARID2: Jumonji AT-rich interactive domain 2; IL-6: Interleukin 6; MAPK: Mitogen-activated protein kinase;
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