Extract
I read with great interest the recent original research article by Wu et al. [1] published in the prestigious European Respiratory Journal (ERJ), which reported on endothelial cell-like myofibroblasts and their role in pulmonary fibrosis using mouse models. I highly commend this work and the focus on endothelial cells in this decidedly fibrotic condition. To further enhance discussion, and to elaborate on the mechanisms involved and contribution of endothelial cells to pulmonary fibrosis, I wish to bring forth some novel insights from our recent work published in ERJ Open Research [2, 3] on idiopathic pulmonary fibrosis (IPF). In these human tissue-based clinical studies, we reported vascular remodelling, extracellular matrix changes and the role of endothelial to mesenchymal transition (EndMT) in driving these pathologies and contribution to fibrosis. These are topical clinical studies on the role of endothelial cells and the process of EndMT in tissue from patients with IPF.
Tweetable abstract
Endothelial to mesenchymal transition (EndMT) is central to pathogenesis of pulmonary fibrosis and a novel therapeutic target. It is now time for “out of the box” thinking to understand this insidious disease. https://bit.ly/43GeetA
Footnotes
Conflict of interest: S.S. Sohal reports honorarium for lectures from Chiesi, travel support from Chiesi, AstraZeneca and GSK, and a research grant from Boehringer Ingelheim, outside the submitted work; and has served on the small airway advisory board for Chiesi Australia for which an honorarium has been received.
Support statement: This work was supported by the Clifford Craig Foundation Launceston General Hospital and Lung Foundation Australia. Funding information for this article has been deposited with the Crossref Funder Registry.
- Received July 12, 2023.
- Accepted July 18, 2023.
- Copyright ©The authors 2023. For reproduction rights and permissions contact permissions{at}ersnet.org