{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Du L"],"funding":["Innovation Plan for Postgraduates of Jiangsu Province","National Natural Science Foundation of China","Natural Science Foundation of the Jiangsu Higher Education Institutions of China"],"pagination":["e2407462"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12005803"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["12(15)"],"pubmed_abstract":["Abnormal proliferation of mesangial cells is a hallmark of diabetic nephropathy (DN). However, the cellular signaling mechanisms that regulate this proliferation remain poorly understood. In this study, it is demonstrated that GA-binding protein (GABP), a member of the ETS family of transcription factors composed of GABPα and GABPβ, plays a significant role in the development of renal fibrosis by modulating mesangial cell proliferation. Notably, the deficiency of GABP in mesangial cells inhibits hyperglycemia-induced proliferation and mitigates renal fibrosis in a murine model of type 2 diabetes mellitus (T2DM). RNA sequencing analysis identifies GLI Family Zinc Finger 1 (GLI1) as the principal downstream effector of GABP in diabetic mice, serving as a crucial regulator of the G1/S transition within the cell cycle. Subsequent investigations have demonstrated that GABP interacts with the GLI1 promoter, facilitating mesangial cell proliferation via GLI1-dependent pathways. This is evidenced by the fact that GLI1 knockdown abrogates the proliferation of mesangial cells with GABP overexpression. Consequently, GABP emerges as a pivotal regulator of renal fibrosis and represents a promising therapeutic target for the treatment of diabetic nephropathy."],"journal":["Advanced science (Weinheim, Baden-Wurttemberg, Germany)"],"pubmed_title":["GABP Promotes Mesangial Cell Proliferation and Renal Fibrosis Through GLI1 in Diabetic Nephropathy."],"pmcid":["PMC12005803"],"funding_grant_id":["82003822","81973377","KYCX19_2252","20KJB310022","82073906"],"pubmed_authors":["Yin X","Hu Y","Zhang J","Lu Y","Liu S","Yang Q","Ren D","Yang T","Du L","Yu X","Lu Q","Ming J"],"additional_accession":[]},"is_claimable":false,"name":"GABP Promotes Mesangial Cell Proliferation and Renal Fibrosis Through GLI1 in Diabetic Nephropathy.","description":"Abnormal proliferation of mesangial cells is a hallmark of diabetic nephropathy (DN). However, the cellular signaling mechanisms that regulate this proliferation remain poorly understood. In this study, it is demonstrated that GA-binding protein (GABP), a member of the ETS family of transcription factors composed of GABPα and GABPβ, plays a significant role in the development of renal fibrosis by modulating mesangial cell proliferation. Notably, the deficiency of GABP in mesangial cells inhibits hyperglycemia-induced proliferation and mitigates renal fibrosis in a murine model of type 2 diabetes mellitus (T2DM). RNA sequencing analysis identifies GLI Family Zinc Finger 1 (GLI1) as the principal downstream effector of GABP in diabetic mice, serving as a crucial regulator of the G1/S transition within the cell cycle. Subsequent investigations have demonstrated that GABP interacts with the GLI1 promoter, facilitating mesangial cell proliferation via GLI1-dependent pathways. This is evidenced by the fact that GLI1 knockdown abrogates the proliferation of mesangial cells with GABP overexpression. Consequently, GABP emerges as a pivotal regulator of renal fibrosis and represents a promising therapeutic target for the treatment of diabetic nephropathy.","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Apr","modification":"2025-07-03T03:04:32.142Z","creation":"2025-07-03T03:04:32.142Z"},"accession":"S-EPMC12005803","cross_references":{"pubmed":["39985381"],"doi":["10.1002/advs.202407462"]}}