{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,5]],"date-time":"2026-11-05T11:00:57Z","timestamp":1793876457579,"version":"4.7.0"},"reference-count":159,"publisher":"Oxford University Press (OUP)","issue":"37","license":[{"start":{"date-parts":[[2023,9,7]],"date-time":"2023-09-07T00:00:00Z","timestamp":1694044800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2023,10,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>For decades, heart failure with preserved ejection fraction (HFpEF) proved an elusive entity to treat. Sodium-glucose cotransporter 2 (SGLT2) inhibitors have recently been shown to reduce the composite of heart failure hospitalization or cardiovascular death in patients with HFpEF in the landmark DELIVER and EMPEROR-Preserved trials. While improvements in blood sugar, blood pressure, and attenuation of kidney disease progression all may play some role, preclinical and translational research have identified additional mechanisms of these agents. The SGLT2 inhibitors have intriguingly been shown to induce a nutrient-deprivation and hypoxic-like transcriptional paradigm, with increased ketosis, erythropoietin, and autophagic flux in addition to altering iron homeostasis, which may contribute to improved cardiac energetics and function. These agents also reduce epicardial adipose tissue and alter adipokine signalling, which may play a role in the reductions in inflammation and oxidative stress observed with SGLT2 inhibition. Emerging evidence also indicates that these drugs impact cardiomyocyte ionic homeostasis although whether this is through indirect mechanisms or via direct, off-target effects on other ion channels has yet to be clearly characterized. Finally, SGLT2 inhibitors have been shown to reduce myofilament stiffness as well as extracellular matrix remodelling\/fibrosis in the heart, improving diastolic function. The SGLT2 inhibitors have established themselves as robust, disease-modifying therapies and as recent trial results are incorporated into clinical guidelines, will likely become foundational in the therapy of HFpEF.<\/jats:p>","DOI":"10.1093\/eurheartj\/ehad389","type":"journal-article","created":{"date-parts":[[2023,9,7]],"date-time":"2023-09-07T06:13:57Z","timestamp":1694067237000},"page":"3640-3651","source":"Crossref","is-referenced-by-count":115,"title":["Mechanisms of benefits of sodium-glucose cotransporter 2 inhibitors in heart failure with preserved ejection fraction"],"prefix":"10.1093","volume":"44","author":[{"given":"Arjun K","family":"Pandey","sequence":"first","affiliation":[{"name":"Michael G. DeGroote School of Medicine, McMaster University, 90 Main Street West, Hamilton, Ontario L8P 1H6, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1278-6245","authenticated-orcid":false,"given":"Deepak L","family":"Bhatt","sequence":"additional","affiliation":[{"name":"Mount Sinai Heart, Icahn School of Medicine at Mount Sinai Health System, 1 Gustave L. Levy Place, New York, NY 10029, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Avinash","family":"Pandey","sequence":"additional","affiliation":[{"name":"Department of Medicine, University of Ottawa Heart Institute, 40 Ruskin St, Ottawa, Ontario K1Y 4W7, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6141-634X","authenticated-orcid":false,"given":"Nikolaus","family":"Marx","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University Hospital Aachen, RWTH Aachen University, Templergraben 55, 52062 Aachen, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6967-5685","authenticated-orcid":false,"given":"Francesco","family":"Cosentino","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, Solna, Karolinska Institutet, Norrbacka S1:02, Stockholm , SE 17177 , Sweden"},{"name":"Heart, 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