ArticleCell death discovery2025
Obesity-associated reduction of miR-150-5p in extracellular vesicles promotes ventilator-induced lung injury by modulating the lysosomal degradation of VE-cadherin.
Article in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Extracellular Vesicles as Drivers of Lung Endothelial Dysfunction in ARDS: Mechanisms and Therapeutic Opportunities.Comprehensive Physiology · 2026Review
- Revisiting ventilator-induced lung injury: from mechanical power to immunometabolic interaction.Frontiers in immunology · 2026Review
- MiR-106a-5p in extracellular vesicles derived from alveolar epithelial cells mediates cognitive dysfunction induced by chronic intermittent hypoxia in mice through MAPK signaling pathway.Journal of neuroinflammation · 2025Article
- MiR-27a-5p deficiency in plasma exosomes derived from obese individuals exacerbates ventilator-induced lung injury in vitro and in vivo.Journal of translational medicine · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Obese patient has a high risk of ventilator-induced lung injury (VILI) but its underlying mechanisms remain elusive. This study was designed to explore the role of circulating plasma extracellular vesicles (EVs) on the progression of VILI in the context of obesity. After high tidal volume mechanical ventilation, mice treated with plasma EVs from obese patients developed more severe lung damage than mice treated with plasma EVs from normal controls. miRNA sequencing of plasma EVs from obese patients revealed a significant downregulation of miR-150-5p compared to the others. miR-150-5p was found to target on XBP1s which subsequently regulated RAB7 as verified through dual-luciferase assays. This pathway promoted lysosomal degradation of vascular endothelial (VE)-cadherin, leading to an increased endothelial permeability. Obese mice showed an enhanced XBP1s/RAB7 expression, reduced VE-cadherin levels, and aggravated endothelial barrier damage and all of which intensified VILI. Administration of miR-150-5p agomir in obese mice mitigated VILI. Thus, this study highlights the low levels of miR-150-5p in EVs from obese patients modulated VILI severity via the XBP1s/RAB7 axis and the lysosomal degradation of VE-cadherin.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.