{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T18:15:23Z","timestamp":1789064123024,"version":"build-2803163510"},"reference-count":86,"publisher":"MDPI AG","issue":"11","license":[{"start":{"date-parts":[[2019,6,11]],"date-time":"2019-06-11T00:00:00Z","timestamp":1560211200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"La Caixa Foundation","award":["HR17-00627"],"award-info":[{"award-number":["HR17-00627"]}]},{"name":"Ministerio de Econom\u00eda y Competitividad\/FEDER-EU","award":["BFU2015-64462R"],"award-info":[{"award-number":["BFU2015-64462R"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Diabetic cardiomyopathy (DCM) has emerged as a relevant cause of heart failure among the diabetic population. Defined as a cardiac dysfunction that develops in diabetic patients independently of other major cardiovascular risks factors, such as high blood pressure and coronary artery disease, the underlying cause of DCMremains to be unveiled. Several pathogenic factors, including glucose and lipid toxicity, mitochondrial dysfunction, increased oxidative stress, sustained activation of the renin-angiotensin system (RAS) or altered calcium homeostasis, have been shown to contribute to the structural and functional alterations that characterize diabetic hearts. However, all these pathogenic mechanisms appear to stem from the metabolic inflexibility imposed by insulin resistance or lack of insulin signaling. This results in absolute reliance on fatty acids for the synthesis of ATP and impairment of glucose oxidation. Glucose is then rerouted to other metabolic pathways, with harmful effects on cardiomyocyte function. Here, we discuss the role that impaired cardiac insulin signaling in diabetic or insulin-resistant individuals plays in the onset and progression of DCM.<\/jats:p>","DOI":"10.3390\/ijms20112833","type":"journal-article","created":{"date-parts":[[2019,6,11]],"date-time":"2019-06-11T10:55:44Z","timestamp":1560250544000},"page":"2833","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":65,"title":["Contribution of Impaired Insulin Signaling to the Pathogenesis of Diabetic Cardiomyopathy"],"prefix":"10.3390","volume":"20","author":[{"given":"M\u00f2nica","family":"Zamora","sequence":"first","affiliation":[{"name":"BCNatal, Fetal Medicine Research Center, Hospital Cl\u00ednic and Hospital Sant Joan de D\u00e9u, University of Barcelona, 08950 Barcelona, Spain"},{"name":"Institut d\u2019Investigacions Biom\u00e8diques August Pi i Sunyer (IDIBAPS), 08036 Barcelona, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2200-2985","authenticated-orcid":false,"given":"Josep A.","family":"Villena","sequence":"additional","affiliation":[{"name":"Laboratory of Metabolism and Obesity, Vall d\u2019Hebron\u2014Institut de Recerca, Universitat Aut\u00f2noma de Barcelona, 08035 Barcelona, Spain"},{"name":"CIBERDEM, CIBER on Diabetes and Associated Metabolic Diseases, Instituto de Salud Carlos III, 28029 Madrid, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2019,6,11]]},"reference":[{"key":"ref_1","unstructured":"World Helath Organization (2019, June 10). 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