Deleted Journal, Journal Year: 2025, Volume and Issue: 2(1), P. 10001 - 10001
Published: Jan. 1, 2025
Idiopathic pulmonary fibrosis (IPF) is a progressive, irreversible, and fatal disease with an increasing incidence limited therapeutic options. It characterized by the formation deposition of excess extracellular matrix proteins resulting in gradual replacement normal lung architecture fibrous tissue. The cellular molecular mechanism IPF has not been fully understood. A hallmark fibroblast to myofibroblast transformation (FMT). During excessive repair upon exposure harmful stimuli, fibroblasts transform into myofibroblasts under stimulation cytokines, chemokines, vesicles from various cells. These mediators interact fibroblasts, initiating multiple signaling cascades, such as TGFβ1, MAPK, Wnt/β-catenin, NF-κB, AMPK, endoplasmic reticulum stress, autophagy, contributing FMT. Furthermore, single-cell transcriptomic analysis revealed significant heterogeneity among myofibroblasts, which arise cell types are adapted altered microenvironment during pathological repair. This review provides overview recent research on origins pathways driving their formation, focus interactions between epithelial cells, endothelial macrophages context fibrosis. Based these insights, targeting FMT could offer promising avenues for treatment IPF.
Language: Английский