{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wu CL"],"funding":["National Science and Technology Council","Changhua Christian Hospital"],"pagination":["e70516"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11936727"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["29(6)"],"pubmed_abstract":["Long-term peritoneal dialysis (PD) leads to peritoneal damage and chronic inflammation, resulting in peritoneal fibrosis (PF). Emerging evidence suggests that yes-associated protein (YAP) is a key player in fibrogenesis across various organs. However, its role in PD-induced PF remains unclear. We used NIH/3T3 cells, primary mouse fibroblasts, and conditional YAP knockout (CKO) mice with glioma-associated oncogene 1 (Gli1)-specific YAP deletion. The effects of YAP knockdown and verteporfin, a YAP inhibitor, on fibroblast-to-mesenchymal transition (FMT) and angiogenesis were evaluated. Transforming growth factor-beta (TGF-β) induced YAP expression and promoted fibroblast-to-myofibroblast transition (FMT) in 3T3 fibroblasts, upregulating collagen 1A1, α-smooth muscle actin (α-SMA), and connec"],"journal":["Journal of cellular and molecular medicine"],"pubmed_title":["Depleting Yes-Associated Protein in Gli1-Expressing Cells Attenuates Peritoneal Dialysis-Induced Peritoneal Fibrosis."],"pmcid":["PMC11936727"],"funding_grant_id":["112-2628-B-371-001","112-CCH-IRP-014","111-2628-B-371-001","112‐CCH‐IRP‐014","110‐2628‐B‐371‐001","110-2628-B-371-001","111‐2628‐B‐371‐001","112‐2628‐B‐371‐001"],"pubmed_authors":["Tsai YL","Wu CL","Hsu JW","Tarng DC","Yu JY","Chan YC"],"additional_accession":[]},"is_claimable":false,"name":"Depleting Yes-Associated Protein in Gli1-Expressing Cells Attenuates Peritoneal Dialysis-Induced Peritoneal Fibrosis.","description":"Long-term peritoneal dialysis (PD) leads to peritoneal damage and chronic inflammation, resulting in peritoneal fibrosis (PF). Emerging evidence suggests that yes-associated protein (YAP) is a key player in fibrogenesis across various organs. However, its role in PD-induced PF remains unclear. We used NIH/3T3 cells, primary mouse fibroblasts, and conditional YAP knockout (CKO) mice with glioma-associated oncogene 1 (Gli1)-specific YAP deletion. The effects of YAP knockdown and verteporfin, a YAP inhibitor, on fibroblast-to-mesenchymal transition (FMT) and angiogenesis were evaluated. Transforming growth factor-beta (TGF-β) induced YAP expression and promoted fibroblast-to-myofibroblast transition (FMT) in 3T3 fibroblasts, upregulating collagen 1A1, α-smooth muscle actin (α-SMA), and connec","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Mar","modification":"2025-07-13T03:04:43.107Z","creation":"2025-07-13T03:04:43.107Z"},"accession":"S-EPMC11936727","cross_references":{"pubmed":["40133213"],"doi":["10.1111/jcmm.70516"]}}