<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zou H</submitter><funding>Special funds for clinical research from Affiliated Qingyuan Hospital, Guangzhou Medical University, Qingyuan People's Hospital</funding><pagination>79</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12801749</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>31(1)</volume><pubmed_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</pubmed_abstract><journal>European journal of medical research</journal><pubmed_title>CILP attenuates pulmonary fibrosis through the TGF-β1/SMAD3 pathway.</pubmed_title><pmcid>PMC12801749</pmcid><funding_grant_id>QYRYCRC2023005</funding_grant_id><pubmed_authors>Zou H</pubmed_authors><pubmed_authors>Li X</pubmed_authors><pubmed_authors>Fei C</pubmed_authors><pubmed_authors>Zhao R</pubmed_authors><pubmed_authors>Dong J</pubmed_authors><pubmed_authors>Li P</pubmed_authors><pubmed_authors>Liu C</pubmed_authors><pubmed_authors>Liu F</pubmed_authors><pubmed_authors>Cheng J</pubmed_authors></additional><is_claimable>false</is_claimable><name>CILP attenuates pulmonary fibrosis through the TGF-β1/SMAD3 pathway.</name><description>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</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-06-10T05:04:16.986Z</modification><creation>2026-06-10T03:07:11.033Z</creation></dates><accession>S-EPMC12801749</accession><cross_references><pubmed>41382307</pubmed><doi>10.1186/s40001-025-03644-7</doi></cross_references></HashMap>