{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Qiao G"],"funding":["National Natural Science Foundation of China"],"pagination":["1452"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12468141"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(18)"],"pubmed_abstract":["Sepsis-induced cardiomyopathy is a life-threatening complication lacking targeted therapies. While empagliflozin (Empa), a sodium-glucose cotransporter 2 (SGLT2) inhibitor, confers robust cardioprotection, its specific efficacy in treating sepsis-induced cardiomyopathy and the Empa mechanisms remain poorly defined, limiting its targeted therapeutic use. In this study, we investigated Empa's effects and its novel mechanisms in a murine lipopolysaccharide (LPS)-induced model of septic cardiomyopathy. Empa pre-treatment effectively prevented LPS-induced cardiac dysfunction, preserving ejection fraction and mitigating myocardial injury (assessed by histology and ELISA) and fibrosis. Transcriptomic analysis revealed that Empa's protective effects were profoundly linked to the preservation of ca"],"journal":["Cells"],"pubmed_title":["Empagliflozin Preserves Cardiomyocyte Structural Homeostasis via the Stabilization of the Integrin α5-Desmocollin-2 Adhesion Axis in Sepsis-Induced Cardiomyopathy."],"pmcid":["PMC12468141"],"funding_grant_id":["No# 82030007 and U23A20398"],"pubmed_authors":["Qiao G","Liang S","Wu J","Liu M","Lu Y","Zhang C","Ren C"],"additional_accession":[]},"is_claimable":false,"name":"Empagliflozin Preserves Cardiomyocyte Structural Homeostasis via the Stabilization of the Integrin α5-Desmocollin-2 Adhesion Axis in Sepsis-Induced Cardiomyopathy.","description":"Sepsis-induced cardiomyopathy is a life-threatening complication lacking targeted therapies. While empagliflozin (Empa), a sodium-glucose cotransporter 2 (SGLT2) inhibitor, confers robust cardioprotection, its specific efficacy in treating sepsis-induced cardiomyopathy and the Empa mechanisms remain poorly defined, limiting its targeted therapeutic use. In this study, we investigated Empa's effects and its novel mechanisms in a murine lipopolysaccharide (LPS)-induced model of septic cardiomyopathy. Empa pre-treatment effectively prevented LPS-induced cardiac dysfunction, preserving ejection fraction and mitigating myocardial injury (assessed by histology and ELISA) and fibrosis. Transcriptomic analysis revealed that Empa's protective effects were profoundly linked to the preservation of ca","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Sep","modification":"2026-05-01T03:22:55.439Z","creation":"2026-05-01T03:11:12.298Z"},"accession":"S-EPMC12468141","cross_references":{"pubmed":["41002417"],"doi":["10.3390/cells14181452"]}}