ArticleAmerican journal of respiratory cell and molecular biology2025
Extracellular Vesicles Contribute to the Pathophysiology and Progression of Pleural Fibrosis by Promoting Mesothelial-to-Mesenchymal Transition and Neoangiogenesis.
Article in American journal of respiratory cell and molecular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Pure isolation, culture, and postinjury lineage tracing of mouse visceral pleural mesothelial cells.American journal of respiratory cell and molecular biology · 2026Article
- Review
- Pathobiology and clinical significance of malignant pleural effusions.EMBO molecular medicine · 2026Review
- Mesothelial Cells in Fibrosis: Focus on Intercellular Crosstalk.Biomolecules · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Severe pleural space inflammation associated with exudative pleural effusions leads to the development of pleural fibrosis (PF). Pathological tissue remodeling in PF is associated with profibrotic changes in the pleural mesothelium and neoangiogenesis within the fibrotic region. However, the factors that promote these processes remain poorly understood. This study investigates the role of extracellular vesicles (EVs) in the development and progression of PF, focusing on mesothelial-to-mesenchymal transition and neoangiogenesis. Human pleural mesothelial cells (HPMCs) were treated with coagulation proteases FXa (factor Xa) and thrombin, and EV production was quantified using nanoparticle tracking analysis. The functional relevance of these EVs was assessed by evaluating their ability to promote a profibrotic phenotype in HPMCs and induce tube formation in endothelial cells. FXa and thrombin treatments significantly increased EV generation from HPMCs via PAR (protease-activated receptor)-mediated cell signaling. Our studies showed that these EVs primed HPMCs toward a profibrotic phenotype and enhanced tube formation in endothelial cells. Further investigations in preclinical mouse models of PF revealed elevated EV levels in pleural fluids from injury-induced mice, compared with saline control mice. In clinical specimens, exudative pleural effusions from patients with empyema and parapneumonic effusions exhibited significantly elevated EV numbers compared with transudative effusions from patients with congestive heart failure. More importantly, EVs isolated from exudative effusions promoted a profibrotic phenotype in naive HPMCs and enhanced tube formation similar to the effects observed with FXa- and thrombin-generated EVs. These findings offer new insights into PF pathogenesis by identifying EVs as previously unknown contributors that modulate mesothelial-to-mesenchymal transition and neoangiogenesis.
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