Afficher la notice abrégée

Empagliflozin inhibits angiotensin II-induced hypertrophy in H9c2 cardiomyoblasts through inhibition of NHE1 expression.

dc.rights.licenseopenen_US
dc.contributor.authorABDULRAHMAN, Nabeel
dc.contributor.authorIBRAHIM, Meram
dc.contributor.authorJOSEPH, Jensa Mariam
dc.contributor.authorELKOUBATRY, Hanan Mahmoud
dc.contributor.authorAL-SHAMASI, Al-Anood
dc.contributor.authorRAYAN, Menatallah
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorGADEAU, Alain Pierre
dc.contributor.authorAHMED, Rashid
dc.contributor.authorELDASSOUKI, Hussein
dc.contributor.authorHASAN, Anwarul
dc.contributor.authorMRAICHE, Fatima
dc.date.accessioned2022-04-07T10:09:56Z
dc.date.available2022-04-07T10:09:56Z
dc.date.issued2022-03-25
dc.identifier.issn1573-4919en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/136605
dc.description.abstractEnDiabetes mellitus (DM)-induced cardiac morbidities have been the leading cause of death among diabetic patients. Recently, sodium-glucose cotransporter-2 (SGLT-2) inhibitors including empagliflozin (EMPA), which have been approved for the treatment of DM, have gained attention for their cardioprotective effect. The mechanism by which SGLT-2 inhibitors exert their cardioprotective effect remains unclear. Recent studies have suggested that EMPA exerts its cardioprotective effect by inhibiting the Na/H exchanger (NHE), a group of membrane proteins that regulate intracellular pH and cell volume. Increased activity and expression of NHE isoform 1 (NHE1), the predominant isoform expressed in the heart, leads to cardiac hypertrophy. p90 ribosomal s6 kinase (p90 RSK) has been demonstrated to stimulate NHE1 activity. In our study, H9c2 cardiomyoblasts were treated with angiotensin II (ANG) to activate NHE1 and generate a hypertrophic model. We aimed to understand whether EMPA reverses the ANG-induced hypertrophic response and to elucidate the molecular pathway contributing to the cardioprotective effect of EMPA. Our study demonstrated that ANG-induced hypertrophy of H9c2 cardiomyoblasts is accompanied with increased SGLT-1 and NHE1 protein expression, an effect which is prevented in the presence of EMPA. EMPA reduces ANG-induced hypertrophy through the inhibition of SGLT-1 and NHE1 expression.
dc.language.isoENen_US
dc.subjectARTICLE RECHERCHE
dc.title.enEmpagliflozin inhibits angiotensin II-induced hypertrophy in H9c2 cardiomyoblasts through inhibition of NHE1 expression.
dc.title.alternativeMol Cell Biochemen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1007/s11010-022-04411-6en_US
dc.identifier.pubmed35334035en_US
bordeaux.journalMolecular and Cellular Biochemistryen_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires (BMC) - UMR 1034en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcepubmed
hal.exportfalse
workflow.import.sourcepubmed
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Molecular%20and%20Cellular%20Biochemistry&rft.date=2022-03-25&rft.eissn=1573-4919&rft.issn=1573-4919&rft.au=ABDULRAHMAN,%20Nabeel&IBRAHIM,%20Meram&JOSEPH,%20Jensa%20Mariam&ELKOUBATRY,%20Hanan%20Mahmoud&AL-SHAMASI,%20Al-Anood&rft.genre=article


Fichier(s) constituant ce document

Thumbnail
Nom:
BMC_Mol. Cell. Biochem._2022_A ...
Taille:
793.4Ko
Format:
PDF
Voir/Ouvrir

Ce document figure dans la(les) collection(s) suivante(s)

Afficher la notice abrégée