{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T23:17:50Z","timestamp":1787008670662,"version":"build-2736575974"},"reference-count":45,"publisher":"Oxford University Press (OUP)","issue":"11","license":[{"start":{"date-parts":[[2019,2,4]],"date-time":"2019-02-04T00:00:00Z","timestamp":1549238400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 HL135000"],"award-info":[{"award-number":["R01 HL135000"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["U01 HL108642"],"award-info":[{"award-number":["U01 HL108642"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["15GRNT25650003"],"award-info":[{"award-number":["15GRNT25650003"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"publisher","award":["16POST27770035"],"award-info":[{"award-number":["16POST27770035"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,9,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Aims<\/jats:title>\n                    <jats:p>We previously reported that sodium-dependent glucose cotransporter 1 (SGLT1) is highly expressed in cardiomyocytes and is further up-regulated in ischaemia. This study aimed to determine the mechanisms by which SGLT1 contributes to ischaemia\/reperfusion (I\/R) injury.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods and results<\/jats:title>\n                    <jats:p>Mice with cardiomyocyte-specific knockdown of SGLT1 (TGSGLT1-DOWN) and wild-type controls were studied. In vivo, the left anterior descending coronary artery was ligated for 30\u2009min and reperfused for 48\u2009h. Ex vivo, isolated perfused hearts were exposed to 20\u2009min no-flow and up to 2\u2009h reperfusion. In vitro, HL-1 cells and isolated adult murine ventricular cardiomyocytes were exposed to 1\u2009h hypoxia and 24\u2009h reoxygenation (H\/R). We found that TGSGLT1-DOWN hearts were protected from I\/R injury in vivo and ex vivo, with decreased infarct size, necrosis, dysfunction, and oxidative stress. 5\u2019-AMP-activated protein kinase (AMPK) activation increased SGLT1 expression, which was abolished by extracellular signal-related kinase (ERK) inhibition. Co-immunoprecipitation studies showed that ERK, but not AMPK, interacts directly with SGLT1. AMPK activation increased binding of the hepatocyte nuclear factor 1 and specificity protein 1 transcription factors to the SGLT1 gene, and HuR to SGLT1 mRNA. In cells, up-regulation of SGLT1 during H\/R was abrogated by AMPK inhibition. Co-immunoprecipitation studies showed that SGLT1 interacts with epidermal growth factor receptor (EGFR), and EGFR interacts with protein kinase C (PKC). SGLT1 overexpression activated PKC and NADPH oxidase 2 (Nox2), which was attenuated by PKC inhibition, EGFR inhibition, and\/or disruption of the interaction between EGFR and SGLT1.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>During ischaemia, AMPK up-regulates SGLT1 through ERK, and SGLT1 interacts with EGFR, which in turn increases PKC and Nox2 activity and oxidative stress. SGLT1 may represent a novel therapeutic target for mitigating I\/R injury.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/cvr\/cvz037","type":"journal-article","created":{"date-parts":[[2019,2,1]],"date-time":"2019-02-01T15:53:27Z","timestamp":1549036407000},"page":"1646-1658","source":"Crossref","is-referenced-by-count":81,"title":["Cardiac sodium-dependent glucose cotransporter 1 is a novel mediator of ischaemia\/reperfusion injury"],"prefix":"10.1093","volume":"115","author":[{"given":"Zhao","family":"Li","sequence":"first","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Internal Medicine, Carver College of Medicine and Abboud Cardiovascular Research Center, University of Iowa, 100 Newton Road, 1191D ML, Iowa City, IA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vineet","family":"Agrawal","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, UPMC Heart and Vascular Institute, University of Pittsburgh, Pittsburgh, PA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mohun","family":"Ramratnam","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, UPMC Heart and Vascular Institute, University of Pittsburgh, Pittsburgh, PA, USA"},{"name":"Cardiology Section, Medical Service, Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin, William. 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Iowa, 100 Newton Road, 1191D ML, Iowa City, IA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xueyin N","family":"Huang","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine, UPMC Heart and Vascular Institute, University of Pittsburgh, Pittsburgh, PA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lindsey","family":"Gifford","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Internal Medicine, Carver College of Medicine and Abboud Cardiovascular Research Center, University of Iowa, 100 Newton Road, 1191D ML, Iowa City, IA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ferhaan","family":"Ahmad","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Medicine, Department of Internal Medicine, Carver College of Medicine and Abboud Cardiovascular Research Center, University of Iowa, 100 Newton Road, 1191D ML, Iowa 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