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AuthorAbdulrahman, Nabeel
AuthorIbrahim, Meram
AuthorJoseph, Jensa Mariam
AuthorElkoubatry, Hanan Mahmoud
AuthorAl-Shamasi, Al Anood
AuthorRayan, Menatallah
AuthorGadeau, Alain Pierre
AuthorAhmed, Rashid
AuthorEldassouki, Hussein
AuthorHasan, Anwarul
AuthorMraiche, Fatima
Available date2023-03-27T10:03:43Z
Publication Date2022-06-01
Publication NameMolecular and Cellular Biochemistry
Identifierhttp://dx.doi.org/10.1007/s11010-022-04411-6
CitationAbdulrahman, N., Ibrahim, M., Joseph, J.M. et al. Empagliflozin inhibits angiotensin II-induced hypertrophy in H9c2 cardiomyoblasts through inhibition of NHE1 expression. Mol Cell Biochem 477, 1865–1872 (2022). https://doi.org/10.1007/s11010-022-04411-6
ISSN03008177
URIhttps://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85127244636&origin=inward
URIhttp://hdl.handle.net/10576/41349
AbstractDiabetes 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.
SponsorOpen Access funding provided by the Qatar National Library. This publication was supported by Qatar University Student Grant No. QUST-2-CPH-2019-9. “The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.”
Languageen
PublisherSpringer
SubjectAngiotensin II
Cardiomyocyte hypertrophy
Empagliflozin
H9c2 cardiomyoblasts
NHE1
SGLT-1/2
TitleEmpagliflozin inhibits angiotensin II-induced hypertrophy in H9c2 cardiomyoblasts through inhibition of NHE1 expression
TypeArticle
Pagination1865-1872
Issue Number6
Volume Number477
ESSN1573-4919
dc.accessType Open Access


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