{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T16:04:11Z","timestamp":1791389051883,"version":"4.3.3"},"reference-count":34,"publisher":"Springer Science and Business Media LLC","issue":"1","license":[{"start":{"date-parts":[[2021,7,2]],"date-time":"2021-07-02T00:00:00Z","timestamp":1625184000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"},{"start":{"date-parts":[[2021,7,2]],"date-time":"2021-07-02T00:00:00Z","timestamp":1625184000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["link.springer.com"],"crossmark-restriction":false},"short-container-title":["Cardiovasc Diabetol"],"published-print":{"date-parts":[[2021,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec>\n                <jats:title>Background<\/jats:title>\n                <jats:p>Myocardial fibrosis is a multistep process, which results in collagen deposition in the injured muscle. Empagliflozin, a sodium-glucose cotransporter 2 inhibitor (SGLT2i), decreases cardiovascular events risk. Little is known on the effects of empagliflozin in non-diabetic patients early post myocardial infarction.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Methods<\/jats:title>\n                <jats:p>Fourteen non-diabetic rats underwent myocardial infarction induction, and treated or not (control)immediately after myocardial infarction by daily empagliflozin (30\u00a0mg\/kg\/day). We evaluated cardiac function at baseline, 2 and 4\u00a0weeks after myocardial infarction by echocardiography, and prior to sacrifice by Millar pressure\u2013volume system. We performed histological and biochemical evaluation of fibrosis and humoral factors promoting fibrosis.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>Baseline ejection fractions were 69.9\u2009\u00b1\u20095.3% and 76.4\u2009\u00b1\u20095.4%, and dropped to final values of 40.1\u2009\u00b1\u20095.8% and 39.4\u2009\u00b1\u20095.4% in the control and empagliflozin groups, respectively (P\u2009&lt;\u20090.001 <jats:italic>vs.<\/jats:italic> baseline, P\u2009&gt;\u20090.05 between groups). Collagen deposition, measured as collagen volume fraction, was higher in both the scar and the remote cardiac areas of the control group 79.1\u2009\u00b1\u20096.2% and 4.6\u2009\u00b1\u20092.5% for control, and 53.8\u2009\u00b1\u20095.4% and 2.5\u2009\u00b1\u20091.3% for empagliflozin group, respectively (P\u2009&lt;\u20090.05 for each). Remote cardiac muscle collagen, measured by hydroxyproline, was 4.1\u2009\u00b1\u20090.4\u00a0\u03bcg\/\u03bcl and 3.6\u2009\u00b1\u20090.2\u00a0\u03bcg\/\u03bcl (P\u2009=\u20090.07). TGF-\u03b21 and Smad3 expression decreased by empagliflozin\u201418.73\u2009\u00b1\u200916.32%, 9.16\u2009\u00b1\u20095.69% and 16.32\u2009\u00b1\u20095.4%, 7.00\u2009\u00b1\u20095.28% in the control and empagliflozin groups, respectively (P\u2009&lt;\u20090.05).<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion\/interpretation<\/jats:title>\n                <jats:p>Empagliflozin administered early after myocardial infarction reduce myocardial fibrosis and inhibit the TGF-\u03b21\/Smad3 fibrotic pathway, probably prior to exerting any hemodynamic or physiological effect.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s12933-021-01322-6","type":"journal-article","created":{"date-parts":[[2021,7,2]],"date-time":"2021-07-02T16:04:07Z","timestamp":1625241847000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":50,"title":["The impact of empagliflozin on cardiac physiology and fibrosis early after myocardial infarction in non-diabetic rats"],"prefix":"10.1186","volume":"20","author":[{"given":"Elias","family":"Daud","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Offir","family":"Ertracht","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nadav","family":"Bandel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gassan","family":"Moady","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Monah","family":"Shehadeh","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tali","family":"Reuveni","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shaul","family":"Atar","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,7,2]]},"reference":[{"key":"1322_CR1","doi-asserted-by":"publisher","first-page":"294","DOI":"10.1177\/1403494819829333","volume":"48","author":"G Sulo","year":"2020","unstructured":"Sulo G, Sulo E, J\u00f8rgensen T, Linnenberg A, Prescott E, Tell GS, et al. 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