Authors
Danni Chen, Fei Xiang
Published in
Canadian respiratory journal. Volume 2026. Issue 1. Pages e6653364.
Abstract
Pulmonary fibrosis (PF) is a progressive fibrotic interstitial lung disease characterized by aberrant activation of myofibroblasts and excessive deposition of extracellular matrix. In light of the complexity of its pathogenesis and the limited availability of approved antifibrotic drugs, PF remains a refractory lung disease imposing a substantial burden on patients. Current research into the pathogenesis of PF has largely revolved around the core hypothesis of recurrent microinjuries to alveolar epithelial cells. However, in recent years, increasing attention has been directed toward the role of endothelial dysfunction in the progression of fibrosis. This review focuses on pulmonary microvascular endothelial cells and systematically examines their regulatory mechanisms in the initiation and progression of PF from three perspectives: endothelial cell senescence and programmed cell death, intercellular crosstalk between endothelial cells and surrounding cells, and endothelial-mesenchymal transition (EndoMT). Furthermore, we summarize antifibrotic drugs and therapeutic strategies targeting endothelial cells, providing theoretical insights and research directions to elucidate the pathogenesis of PF and explore novel therapeutic approaches.
PMID:
42357969
Bibliographic data and abstract were imported from PubMed on 13 Sep 2026.
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