Extract
Fibroblasts within the stroma play a crucial role in tissue architecture homeostasis. These mesenchymal cells are at the front line after tissue injury to support epithelial repair through their differentiation into “physiological” myofibroblasts, followed by their programmed dismissal at the end of the process [1, 2]. Chronic injuries may lead to unbalanced cell–cell communication that would promote the persistence of activated “pathological” myofibroblasts and hence excessive accumulation of extracellular matrix (ECM) components, one of the salient marks of fibrosis. In the lung, interstitial fibrosis leads to alveolar destruction and lung function decline. Idiopathic pulmonary fibrosis (IPF) is the most frequent form of interstitial lung disease, with a median overall survival time of 4.5 years.
Abstract
Identification of MDB2 as a critical interpreter of DNA methylation during myofibroblastic differentiation downstream of TGF-β1 signalling pathway in lung fibrosis https://bit.ly/3BIJbCW
Footnotes
Conflict of interest: A.A. Mailleux has nothing to disclose. B. Crestani has received personal fees and non-financial support from AstraZeneca, Apelis and Sanofi, grants, personal fees and non-financial support from Boehringer Ingelheim, non-financial support from Cardif and lvl, and grants from MedImmune.
- Received August 2, 2022.
- Accepted August 8, 2022.
- Copyright ©The authors 2022. For reproduction rights and permissions contact permissions{at}ersnet.org
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