ArticleJournal of translational medicine2025
MiR-27a-5p deficiency in plasma exosomes derived from obese individuals exacerbates ventilator-induced lung injury in vitro and in vivo.
Article in Journal of translational medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Revisiting ventilator-induced lung injury: from mechanical power to immunometabolic interaction.Frontiers in immunology · 2026Review
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9 authors.
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Abstract
backgroundVentilator-induced lung injury (VILI) frequently occurs in obese individuals and significantly negates outcomes. Understanding mechanisms behind susceptibility of obese patients to VILI is, therefore, important. This study delved into the molecular biology mechanisms of VILI and investigated the effects of plasma exosomes from obese patients on VILI in mice, as well as its potential molecular mechanisms.
methodsMicroRNAs (miRNAs) in plasma-derived exosomes from 6 obese patients and 6 healthy volunteers were analysed to map different miRNA profiles. A lung cell line (MLE-12) was cultured with or without exosomes from obese patients and then challenged with cyclic stretching for 4 h. Western blotting, immunofluorescence, electron microscopy and other techniques were used to detect intercellular connections directly or indirectly. Co-immunoprecipitation and dual luciferase reporter experiments were conducted to verify underlying mechanism involved. Lung function, wet/dry (W/D) ratio, pathological changes, and inflammatory cytokines in alveolar lavage fluid were measured in C57BL/6 mice after 4 h of mechanical ventilation with high tidal volume.
resultsCompared to those in healthy volunteers, miR-27a-5p was decreased in plasma exosomes from obese patients. Cyclic stretching induces endoplasmic reticulum (ER) stress in lung cells and consequently promotes the generation of Xbp1s, which act as transcription factors to initiate the phosphorylation of proline-rich tyrosine kinase 2 (Pyk2). p-Pyk2 thereby activated hepatocyte growth factor-regulated tyrosine kinase substrate (Hgs), which, in turn, promoted the endocytosis and transport of E-cadherin for lysosomal degradation and subsequently disrupted the pulmonary epithelial barrier. miR-27a-5p administered to cultured lung cells and mice protected lung cells and attenuated VILI through the regulation of Pyk2.
conclusionOur findings suggest that the increased susceptibility of obese patients to VILI is likely, at least in part, due to a lack of miR-27a-5p in plasma exosomes. Targeting miR-27a-5p and its associated molecules may be a promising therapeutic avenue for preventing and treating VILI in obese patients.
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