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Empagliflozin modulates microRNA expression in human primary cardiomyocytes under CoCl2-induced hypoxia
Marek Samec1, Ivana Baranova2, Katarina Dibdiakova3
1Department of Medical Biology, Jessenius Faculty of Medicine in Martin, Comenius University Bratislava, Martin, Slovakia.
Insights
Empagliflozin, an SGLT2 inhibitor, shows cardioprotective effects by upregulating miR-214-3p in hypoxic cardiomyocytes. This suggests Empagliflozin may act as an epigenetic modulator in cardiovascular disease (CVD) pathogenesis.
Area of Science:
- Cardiology
- Molecular Biology
- Pharmacology
Background:
- Cardiovascular diseases (CVD) are a leading cause of global mortality.
- Ischemia and hypoxia in CVD cause cellular damage and epigenetic alterations.
- Empagliflozin (SGLT2 inhibitor) shows promise in treating CVD.
Purpose of the Study:
- To investigate Empagliflozin's protective role in human cardiomyocytes under hypoxia.
- To analyze Empagliflozin's effect on specific microRNAs (miRNAs) and proteins.
Main Methods:
- Primary human cardiomyocytes were exposed to chemically induced hypoxia.
- Cells were treated with Empagliflozin for 24 hours.
- Expression of miR-214-3p, miR-22-5p, miR-103-5p, miR-145-5p, GAPDH, and HIF1α was analyzed.
Main Results:
- Empagliflozin treatment significantly upregulated cardioprotective miR-214-3p (p < 0.05).
- This indicates a direct protective effect of Empagliflozin on cardiomyocytes under stress.
Conclusions:
- Empagliflozin exhibits direct cardioprotective effects in hypoxic cardiomyocytes.
- Empagliflozin may function as an epigenetic modulator in CVD development.
Background:
Cardiovascular diseases (CVD) remain the leading cause of premature death worldwide, with a steadily rising incidence. Ischemia, characterized by insufficient blood flow and subsequent tissue hypoxia, contributes significantly to cellular damage, dysfunction, as well as epigenetic alterations in CVD. Hypoxia-induced epigenetic changes have been associated with fibrosis, inflammation, metabolic dysregulation, and altered programmed cell death in cardiac tissue. Empagliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor primarily prescribed for type 2 diabetes, has also demonstrated beneficial effects in patients with CVD.
Methods:
The present study aimed to evaluate the protective role of Empagliflozin in primary human cardiomyocytes under chemically induced hypoxia, with a focus on its influence on specific microRNAs. Cardioprotective effects were analyzed through the expression of miR-214-3p, miR-22-5p, miR-103-5p, and miR-145-5p, along with protein levels of GAPDH and HIF1α.
Results And Conclusion:
After 24 h of Empagliflozin treatment, a significant upregulation of the cardioprotective miR-214-3p (p < 0.05) was observed. These findings demonstrate a direct cardioprotective effect of Empagliflozin in cobalt-treated cardiomyocytes and suggest its potential role as an epigenetic modulator in the pathogenesis of CVD.
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