Evidence for a lipofibroblast-to-<i>Cthrc1</i> ⁺ myofibroblast reversible switch during the development and resolution of lung fibrosis in young mice.

ABSTRACT:

Background

Fibrosis is often associated with aberrant repair mechanisms that ultimately lead to organ failure. In the lung, idiopathic pulmonary fibrosis (IPF) is a fatal form of interstitial lung disease for which there is currently no curative therapy. From the cell biology point of view, the cell of origin and eventual fate of activated myofibroblasts (aMYFs) have taken centre stage, as these cells are believed to drive structural remodelling and lung function impairment. While aMYFs are now widely believed to originate from alveolar fibroblasts, the heterogeneity and ultimate fate of aMYFs during fibrosis resolution remain elusive. We have shown previously that aMYF dedifferentiation and acquisition of a lipofibroblast (LIF)-like phenotype represent a route of fibrosis resoluti

SUBMITTER: Lingampally A 

PROVIDER: S-EPMC11799885 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature