CILP attenuates pulmonary fibrosis through the TGF-β1/SMAD3 pathway.

ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a chronic progressive disease with poor survival, which is characterized by abnormal accumulation of fibrotic tissue in the lung parenchyma. Transforming growth factor-β1 (TGF-β) is a central profibrotic mediator, but the related mechanism of the activation of latent TGF-β has not been conclusively elucidated. A comprehensive study of mRNAs in human IPF was conducted using GSE10667 microarray data from GEO database, and the expression of cartilage intermediate layer protein (CILP) was upregulated among end-stage pulmonary fibrosis (EPF) and acute pulmonary fibrosis (APF) as compared to non-fibrosis tissues. Furthermore, CILP has protein-protein interactions with TGF-β1 through PPI analysis. Therefore, we investigated the potential effects and mechanis

SUBMITTER: Zou H 

PROVIDER: S-EPMC12801749 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature