<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>13</volume><submitter>Guo R</submitter><funding>National Natural Science Foundation of China Science and Technology Innovation Talents in Universities of Henan Province</funding><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</pubmed_abstract><journal>Frontiers in pharmacology</journal><pagination>897167</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9550168</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>SGLT2 inhibitors suppress epithelial-mesenchymal transition in podocytes under diabetic conditions &lt;i>via&lt;/i> downregulating the IGF1R/PI3K pathway.</pubmed_title><pmcid>PMC9550168</pmcid><pubmed_authors>Wang P</pubmed_authors><pubmed_authors>Zheng X</pubmed_authors><pubmed_authors>Cui W</pubmed_authors><pubmed_authors>Shang J</pubmed_authors><pubmed_authors>Guo R</pubmed_authors><pubmed_authors>Zhao Z</pubmed_authors></additional><is_claimable>false</is_claimable><name>SGLT2 inhibitors suppress epithelial-mesenchymal transition in podocytes under diabetic conditions &lt;i>via&lt;/i> downregulating the IGF1R/PI3K pathway.</name><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</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2026-06-22T03:18:54.909Z</modification><creation>2026-06-22T03:08:41.146Z</creation></dates><accession>S-EPMC9550168</accession><cross_references><pubmed>36225569</pubmed><doi>10.3389/fphar.2022.897167</doi></cross_references></HashMap>