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Empagliflozin improves post-infarction cardiac remodeling through GTP enzyme cyclohydrolase 1 and irrespective of diabetes status

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dc.contributor.authorAsensio Lopez, Maria del Carmen
dc.contributor.authorLax PĂ©rez, Antonio Manuel
dc.contributor.authorHernandez Vicente, Alvaro
dc.contributor.authorSaura Guillen, Elena
dc.contributor.authorHernandez Martinez, Antonio
dc.contributor.authorFernandez del Palacio, Maria J
dc.contributor.authorBayes Genis, Antoni
dc.contributor.authorPascual Figal, Domingo A.
dc.contributor.departmentMedicina
dc.date.accessioned2024-01-23T08:11:24Z
dc.date.available2024-01-23T08:11:24Z
dc.date.issued2020-08
dc.description©2020. This manuscript version is made available under the CC-BY 4.0 license http://creativecommons.org/licenses/by/4.0/ This document is the Published, version of a Published Work that appeared in final form in Scientific Reports. To access the final edited and published work see https://doi.org/10.1038/s41598-020-70454-8es
dc.description.abstractSodium-glucose co-transporter-2 inhibitors (SGLT2i) have shown to prevent heart failure progression, although the mechanisms remain poorly understood. Here we evaluated the effect of empagliflozin (EMPA, SGLT2i) in cardiac remodeling after myocardial infarction, the interplay with diabetes status and the role of cardiac GTP enzyme cyclohydrolase 1 (cGCH1). A rat model of diabetes (50 mg/kg streptozotocin, i.p.) was subjected to myocardial infarction and left ventricular systolic dysfunction, by ligation of the left anterior descending coronary artery. EMPA therapy significantly improved cardiac remodeling parameters and ameliorated processes of fibrosis and hypertrophy, in both non-diabetic and diabetic rats. This cardioprotective effect related with a significant increase in myocardial expression levels of cGCH1, which led to activation of nNOS and eNOS, and inhibition of iNOS, and subsequently resulted in increasing of NO levels and decreasing O2.- and nitrotyrosine levels. These effects were replicated in a cardiomyocyte biomechanical stretching diabetic model, where silencing cGCH1 blocked the preventive effect of EMPA. The beneficial effects were observed irrespective of diabetes status, although the magnitude was greater in presence of diabetes. Empagliflozin improves myocardial remodeling after myocardial infarction through overexpression of cGCH1, and irrespective of diabetes status.es
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dc.format.extent14es
dc.identifier.citationScientific Reports
dc.identifier.doihttps://doi.org/10.1038/s41598-020-70454-8
dc.identifier.issn2045-2322
dc.identifier.urihttp://hdl.handle.net/10201/137554
dc.languageenges
dc.relationThis study was supported by a grant from the Seneca Foundation-Agency of Science and Technology of the Region of Murcia (20652/JLI/18) and a grant from the Instituto de Salud Carlos III (PI19/00519). Dr. Lax is a recipient of a research contract to the Spanish System of Science, Technology and Innovation by the University of Murcia.es
dc.rightsinfo:eu-repo/semantics/openAccesses
dc.rightsAtribuciĂłn 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.titleEmpagliflozin improves post-infarction cardiac remodeling through GTP enzyme cyclohydrolase 1 and irrespective of diabetes statuses
dc.typeinfo:eu-repo/semantics/articlees
dspace.entity.typePublicationes
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