TMEM176B Prevents and alleviates bleomycin-induced pulmonary fibrosis via inhibiting transforming growth factor β-Smad signaling.

ABSTRACT: Pulmonary fibrosis is a severe and progressive lung disease characterized by the abnormal accumulation of extracellular matrix, leading to scarring and loss of normal lung function. Recent bioinformatics analysis through the Gene Expression Omnibus (GEO) database identified a significant downregulation of Transmembrane Protein 176B (TMEM176B), previously unexplored in the context of fibrotic lung tissues. To investigate the functional role of TMEM176B, we induced pulmonary fibrosis in mice using bleomycin, TGFβ1, and silica, which consistently resulted in a marked decrease in TMEM176B expression. Intriguingly, overexpression of TMEM176B via adenoviral vectors prior to the induction of fibrosis led to significant improvements in fibrotic manifestations and lung function. Mechanistically, TM

SUBMITTER: Wang Z 

PROVIDER: S-EPMC11336771 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature