ArticleAmerican journal of respiratory cell and molecular biology2025
von Willebrand Factor Deficiency Inhibits Endothelial-to-Mesenchymal Transition to Attenuate Pulmonary Fibrosis.
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 2 papers.
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Who cites it
2 citing papers in PubMed.
- The Endothelial Cell Perspective in Pulmonary Fibrosis: From Cell Fate Decisions, Intercellular Communication, and EndoMT to Emerging Therapies.Canadian respiratory journal · 2026Review
- von Willebrand Factor: An Unhealthy Bond between Lung Endothelium and Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2025Article
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9 authors.
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Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, interstitial lung disease lacking an efficient drug to reverse it. Thus, there is an urgent need to elucidate the complex pathogenesis of IPF and identify new therapeutic targets. It has been revealed that the pathophysiology of IPF is a highly orchestrated process that includes multiple cell types in which the contribution of endothelial cells (ECs) has attracted researchers' attention. However, although the involvement of ECs in fibrosis has been recognized, the underlying key molecules driving these changes are not well defined. In this study, we revealed that von Willebrand factor (VWF), a marker of damaged ECs, and endothelial dysfunction are positively correlated with IPF progression on the basis of reanalysis of gene expression profiles of patients with IPF. Next, we discovered that
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