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Empagliflozin, a sodium-glucose cotransporter-2 (SGLT2) inhibitor, provides cardiovascular benefits for patients with HFpEF. SGLT2 expression is virtually absent in cardiomyocytes, hence the exact protective mechanism of empagliflozin is unclear. We aimed to study the effect of in vivo empagliflozin treatment on excitation\u2013contraction coupling (ECC), electrophysiology, and gene transcription in a translational two-hit HFpEF mouse model that combines the obese-diabetic leptin receptor-deficient\n                    <jats:italic>db\/db<\/jats:italic>\n                    mice with chronic aldosterone infusion (\n                    <jats:italic>db\/db<\/jats:italic>\n                    \u2009+\u2009Aldo). We performed morphometry, echocardiography, cardiomyocyte electrophysiology, intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    imaging, and whole-heart RNA-sequencing in empagliflozin-treated\n                    <jats:italic>db\/db<\/jats:italic>\n                    \u2009+\u2009Aldo and vehicle control mice. In\n                    <jats:italic>db\/db<\/jats:italic>\n                    \u2009+\u2009Aldo mice, empagliflozin (in vivo, 4 weeks) reduced the elevated plasma blood glucose (13\u2009\u00b1\u20095 mmol\/L\n                    <jats:italic>versus<\/jats:italic>\n                    23\u2009\u00b1\u20098 mmol\/L) and BNP levels, prevented pulmonary congestion, and ameliorated diastolic dysfunction. However, empagliflozin did not reduce cardiac hypertrophy and obesity. In healthy control mice, empagliflozin had no functional effect. Chronic in vivo empagliflozin treatment in\n                    <jats:italic>db\/db<\/jats:italic>\n                    \u2009+\u2009Aldo also normalized the changes in cardiomyocyte electrophysiology and Ca\n                    <jats:sup>2+<\/jats:sup>\n                    handling properties measured in the absence of empagliflozin in the perfusion solution during cell experiments, indicating a true phenotypic rescue. Differentially expressed gene clusters were identified characteristic of the\n                    <jats:italic>db\/db<\/jats:italic>\n                    genotype, aldosterone, and empagliflozin treatments. Interestingly, empagliflozin did not just reverse the HFpEF-altered gene expression but shifted it further away from control to a new expression profile. We conclude that chronic in vivo empagliflozin treatment restores cardiomyocyte electrophysiological and ECC properties, ameliorates diastolic function in cardiometabolic HFpEF, and induces complex gene expression changes.\n                  <\/jats:p>","DOI":"10.1007\/s00395-026-01184-7","type":"journal-article","created":{"date-parts":[[2026,5,21]],"date-time":"2026-05-21T15:38:15Z","timestamp":1779377895000},"page":"669-688","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Empagliflozin restores cardiac function in obese-diabetic HFpEF mice but further alters gene expression"],"prefix":"10.1007","volume":"121","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6689-4284","authenticated-orcid":false,"given":"Juliana","family":"Mira Hernandez","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-7811-7362","authenticated-orcid":false,"given":"Logan R. 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