Why the study?
To determine whether empagliflozin reduces ventricular fibrillation and myocardial fibrosis after myocardial infarction via the transforming growth factor-beta1/Smad3/miR-181a pathway.
Does empagliflozin reduce ventricular fibrillation and myocardial fibrosis in a rat model of myocardial infarction?
Does empagliflozin reduce ventricular fibrillation and myocardial fibrosis in a rat model of myocardial infarction?
Empagliflozin attenuates post-myocardial infarction ventricular arrhythmias and fibrosis in a rat model, highlighting its therapeutic potential in post-infarct remodeling.
Answers are grounded in this paper and cite their sources.
Empagliflozin may raise VF threshold and lessen fibrosis post-MI in rats; leaves open clinical translation and human mechanism confirmation.
ObjectiveTo determine whether empagliflozin reduces ventricular fibrillation and myocardial fibrosis after myocardial infarction via the transforming growth factor-β1/Smad3/miR-181a pathway.MethodsMale nondiabetic Sprague-Dawley rats (n = 16) were randomized into sham, myocardial infarction, low-dose empagliflozin (10 mg/kg/day), and high-dose empagliflozin (30 mg/kg/day) groups. Myocardial infarction was induced via coronary artery ligation. After 4 weeks, ventricular fibrillation thresholds were assessed via electrical stimulation. Cardiac function (echocardiography), fibrosis (Masson's trichrome staining), and molecular markers (transforming growth factor-β1, Smad3, miR-181a; assessed via western blotting/quantitative polymerase chain reaction) were analyzed.ResultsEmpagliflozin-treated groups showed reduced left ventricular dilation (left ventricular internal diameters at end-diastole: 8.2 ± 0.3 vs. 9.1 ± 0.4 mm in myocardial infarction; left ventricular internal diameters at end-systole: 5.1 ± 0.2 vs. 6.0 ± 0.3 mm) and improved ejection fraction (45% vs. 38% in myocardial infarction). Ventricular fibrillation thresholds increased significantly with empagliflozin administration (p < 0.05). Myocardial fibrosis (collagen volume fraction: 12% vs. 25% in myocardial infarction) and transforming growth factor-β1/Smad3/miR-181a expression were downregulated in empagliflozin groups (p < 0.01). No dose-dependent differences were observed between the groups.ConclusionsEmpagliflozin attenuates postmyocardial infarction ventricular arrhythmias and fibrosis associated with the suppression of transforming growth factor-β1/Smad3 signaling and miR-181a expression, enhancing cardiac function. These findings highlight its therapeutic potential in postinfarct remodeling.
No takes yet. Share an insight, caveat, or question.
Shen et al. (2025) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: