ArticleJournal of cachexia, sarcopenia and muscle2026
Cigarette Smoke-Exposed Alveolar Epithelial Cell-Derived Exosomes Exacerbate Skeletal Muscle Dysfunction Through HDAC2 Signalling.
Article in Journal of cachexia, sarcopenia and muscle, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundSkeletal muscle dysfunction (SMD) is a common extrapulmonary complication of chronic obstructive pulmonary disease (COPD). Histone deacetylase 2 (HDAC2) is closely involved in the suppression of inflammatory transcription and is progressively reduced during COPD progression. Exosomes mediate intercellular communication by transferring bioactive cargos, including proteins. This study aimed to elucidate the molecular mechanism by which alveolar epithelial cell-derived exosomes regulate HDAC2 and contribute to COPD-related SMD.
methodsExosome inhibitor GW4869 was used to assess the role of exosomes in skeletal muscle injury induced by chronic cigarette smoke (CS) exposure. Exosomes isolated from the bronchoalveolar lavage fluid (BALF) of CS-exposed mice and from cigarette smoke extract (CSE)-exposed mouse alveolar epithelial (MLE12) cells were applied to recipient mice and/or mouse myoblast (C2C12) cells to evaluate muscle phenotypes, myogenic differentiation and cellular senescence. Rescue experiments using HDAC2 overexpression or HDAC activator ITSA1 treatment, together with proteomics and protein interaction assays, were performed to elucidate the underlying molecular mechanisms.
resultsGW4869 treatment ameliorated CS-induced muscle dysfunction in mice, as evidenced by increased grip strength (222.4 ± 15.91 g vs. 159.2 ± 11.65 g, p < 0.001) and muscle fibre cross-sectional area (404.0 ± 5.15 μm
conclusionsIn COPD, CS-exposed alveolar epithelial cells release PRELP-enriched exosomes that promote SMD by disrupting HSPA5-mediated HDAC2 stabilization and accelerating HDAC2 degradation. Targeting the PRELP-HDAC2 axis may represent a potential therapeutic strategy for COPD-related SMD.
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