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Finerenone ameliorated ventricular remodeling post myocardial infarction in rats by reducing NF-KB pathway-mediated
Xue Sun1, Linlin Song1, Qipei Liu1
1Department of Cardiology, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang, 150001, China.
Abstract:
Myocardial infarction (MI) remains a leading cardiovascular cause of mortality in patients, primarily driven by adverse post-MI ventricular remodeling tightly linked to inflammation. Finerenone, the first non-steroidal mineralocorticoid receptor (MR) antagonist, is clinically indicated to improve cardiovascular and renal outcomes in patients with chronic kidney disease (CKD) associated with type 2 Diabetes Mellitus (T2DM). Multiple previous studies have validated the robust cardioprotective effects of finerenone post MI. Nevertheless, whether finerenone ameliorates post-MI ventricular remodeling by regulating pyroptosis, an inflammation-associated programmed cell death, and its specific underlying molecular mechanisms remain largely uncharacterized. Male Sprague-Dawley (SD) rats were randomly divided into Sham group, MI group, MI + Spironolactone group and MI + Finerenone group. Compared with MI group, finerenone ameliorated ventricular remodeling and inhibited inflammatory cell infiltration post MI in rats. Meanwhile, finerenone reduced myocardial MR expression, pyroptosis and activation of NF-κB signaling pathway post MI in rats. The in vitro experimental results further showed finerenone could inhibit pyroptosis through MR-activated NF-κB pathway. Finerenone could reduce cardiac inflammation and improve ventricular remodeling post MI probably by decreasing NF-κB signaling pathway mediated pyroptosis via MR, which offer promising a novel therapeutic target for clinical intervention in patients with MI.
Insights
Finerenone, a mineralocorticoid receptor antagonist, reduces cardiac inflammation and improves ventricular remodeling after myocardial infarction (MI) in rats. It likely works by inhibiting pyroptosis, a programmed cell death linked to inflammation, via the NF-κB pathway.
Area of Science:
- Cardiology
- Molecular Biology
- Pharmacology
Background:
- Myocardial infarction (MI) leads to adverse ventricular remodeling driven by inflammation.
- Finerenone is a mineralocorticoid receptor (MR) antagonist approved for chronic kidney disease (CKD) in type 2 diabetes (T2DM).
- Previous studies show finerenone's cardioprotective effects post-MI, but its impact on pyroptosis remains unclear.
Purpose of the Study:
- To investigate if finerenone ameliorates post-MI ventricular remodeling by regulating pyroptosis.
- To elucidate the molecular mechanisms underlying finerenone's effects on pyroptosis post-MI.
Main Methods:
- Male Sprague-Dawley rats were divided into Sham, MI, MI + Spironolactone, and MI + Finerenone groups.
- Evaluated ventricular remodeling, inflammatory cell infiltration, and myocardial MR expression.
- Assessed pyroptosis and NF-κB signaling pathway activation.
- Conducted in vitro experiments to confirm pyroptosis inhibition via the MR-NF-κB pathway.
Main Results:
- Finerenone significantly ameliorated ventricular remodeling and reduced inflammatory cell infiltration post-MI.
- Finerenone decreased myocardial MR expression, pyroptosis, and NF-κB pathway activation.
- In vitro studies confirmed finerenone inhibits pyroptosis through the MR-activated NF-κB pathway.
Conclusions:
- Finerenone reduces cardiac inflammation and improves ventricular remodeling post-MI in rats.
- This effect is likely mediated by decreasing NF-κB signaling pathway-driven pyroptosis via MR.
- Finerenone presents a potential novel therapeutic target for clinical intervention in MI patients.
