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dc.rights.licenseopenen_US
dc.contributor.authorAL-SHAMASI, Al-Anood
dc.contributor.authorELKAFFASH, Rozina
dc.contributor.authorMOHAMED, Meram
dc.contributor.authorRAYAN, Menatallah
dc.contributor.authorAL-KHATER, Dhabya
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorGADEAU, Alain-Pierre
dc.contributor.authorAHMED, Rashid
dc.contributor.authorHASAN, Anwarul
dc.contributor.authorELDASSOUKI, Hussein
dc.contributor.authorYALCIN, Huseyin Cagatay
dc.contributor.authorABDUL-GHANI, Muhammad
dc.contributor.authorMRAICHE, Fatima
dc.date.accessioned2022-02-03T16:29:04Z
dc.date.available2022-02-03T16:29:04Z
dc.date.issued2021-11-24
dc.identifier.issn1422-0067en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/124665
dc.description.abstractEnAbnormality in glucose homeostasis due to hyperglycemia or insulin resistance is the hallmark of type 2 diabetes mellitus (T2DM). These metabolic abnormalities in T2DM lead to cellular dysfunction and the development of diabetic cardiomyopathy leading to heart failure. New antihyperglycemic agents including glucagon-like peptide-1 receptor agonists and the sodium-glucose cotransporter-2 inhibitors (SGLT2i) have been shown to attenuate endothelial dysfunction at the cellular level. In addition, they improved cardiovascular safety by exhibiting cardioprotective effects. The mechanism by which these drugs exert their cardioprotective effects is unknown, although recent studies have shown that cardiovascular homeostasis occurs through the interplay of the sodium-hydrogen exchangers (NHE), specifically NHE1 and NHE3, with SGLT2i. Another theoretical explanation for the cardioprotective effects of SGLT2i is through natriuresis by the kidney. This theory highlights the possible involvement of renal NHE transporters in the management of heart failure. This review outlines the possible mechanisms responsible for causing diabetic cardiomyopathy and discusses the interaction between NHE and SGLT2i in cardiovascular diseases.
dc.language.isoENen_US
dc.subject.enAnimals
dc.subject.enCardiovascular Diseases
dc.subject.enDiabetes Mellitus
dc.subject.enType 2
dc.subject.enDiabetic Cardiomyopathies
dc.subject.enHumans
dc.subject.enSodium-Glucose Transporter 2 Inhibitors
dc.subject.enSodium-Hydrogen Exchangers
dc.title.enCrosstalk between Sodium-Glucose Cotransporter Inhibitors and Sodium-Hydrogen Exchanger 1 and 3 in Cardiometabolic Diseases.
dc.title.alternativeInt J Mol Scien_US
dc.typeArticle de revueen_US
dc.identifier.doi10.3390/ijms222312677en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologie/Cardiologie et système cardiovasculaireen_US
dc.identifier.pubmed34884494en_US
bordeaux.journalInternational Journal of Molecular Sciencesen_US
bordeaux.volume22en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires (BMC) - UMR 1034en_US
bordeaux.issue23en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcepubmed
hal.identifierhal-03555699
hal.version1
hal.date.transferred2022-02-03T16:29:08Z
hal.exporttrue
workflow.import.sourcepubmed
dc.rights.ccCC BYen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=International%20Journal%20of%20Molecular%20Sciences&rft.date=2021-11-24&rft.volume=22&rft.issue=23&rft.eissn=1422-0067&rft.issn=1422-0067&rft.au=AL-SHAMASI,%20Al-Anood&ELKAFFASH,%20Rozina&MOHAMED,%20Meram&RAYAN,%20Menatallah&AL-KHATER,%20Dhabya&rft.genre=article


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