{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["13"],"submitter":["Guo R"],"funding":["National Natural Science Foundation of China Science and Technology Innovation Talents in Universities of Henan Province"],"pubmed_abstract":["Loss of podocyte is a characteristic pathological change of diabetic nephropathy (DN) which is associated with increased proteinuria. Many studies have shown that novel inhibitors of sodium-glucose cotransporter 2 (SGLT2-is), such as dapagliflozin, exert nephroprotective effect on delaying DN progression. However, the mechanisms underlying SGLT2-associated podocyte injury are still not fully elucidated. Here, we generated streptozotocin-induced DN models and treated them with dapagliflozin to explore the possible mechanisms underlying SGLT2 regulation. Compared to mice with DN, dapagliflozin-treated mice exhibited remission of pathological lesions, including glomerular sclerosis, thickening of the glomerular basement membrane (GBM), podocyte injury in the glomeruli, and decreased nephrotox"],"journal":["Frontiers in pharmacology"],"pagination":["897167"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9550168"],"repository":["biostudies-literature"],"pubmed_title":["SGLT2 inhibitors suppress epithelial-mesenchymal transition in podocytes under diabetic conditions <i>via</i> downregulating the IGF1R/PI3K pathway."],"pmcid":["PMC9550168"],"pubmed_authors":["Wang P","Zheng X","Cui W","Shang J","Guo R","Zhao Z"],"additional_accession":[]},"is_claimable":false,"name":"SGLT2 inhibitors suppress epithelial-mesenchymal transition in podocytes under diabetic conditions <i>via</i> downregulating the IGF1R/PI3K pathway.","description":"Loss of podocyte is a characteristic pathological change of diabetic nephropathy (DN) which is associated with increased proteinuria. Many studies have shown that novel inhibitors of sodium-glucose cotransporter 2 (SGLT2-is), such as dapagliflozin, exert nephroprotective effect on delaying DN progression. However, the mechanisms underlying SGLT2-associated podocyte injury are still not fully elucidated. Here, we generated streptozotocin-induced DN models and treated them with dapagliflozin to explore the possible mechanisms underlying SGLT2 regulation. Compared to mice with DN, dapagliflozin-treated mice exhibited remission of pathological lesions, including glomerular sclerosis, thickening of the glomerular basement membrane (GBM), podocyte injury in the glomeruli, and decreased nephrotox","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022","modification":"2026-06-22T03:18:54.909Z","creation":"2026-06-22T03:08:41.146Z"},"accession":"S-EPMC9550168","cross_references":{"pubmed":["36225569"],"doi":["10.3389/fphar.2022.897167"]}}