Finerenone Attenuates Myocardial Fibrosis and Pyroptosis in Rats with Myocardial Infarction.
J, W., YC, O., HH, K., YQ, L., LM, L., & JY, L. (2026). Finerenone Attenuates Myocardial Fibrosis and Pyroptosis in Rats with Myocardial Infarction.. International heart journal. https://doi.org/10.1536/ihj.25-278
J W, YC O, HH K, YQ L, LM L, JY L. Finerenone Attenuates Myocardial Fibrosis and Pyroptosis in Rats with Myocardial Infarction.. International heart journal. 2026; doi: 10.1536/ihj.25-278
J W, YC O, HH K, et al. Finerenone Attenuates Myocardial Fibrosis and Pyroptosis in Rats with Myocardial Infarction.[J]. International heart journal. 2026. DOI: 10.1536/ihj.25-278.
@article{j2026,
author = {Wen J and Ou YC and Ke HH and Lu YQ and Liang LM and Li JY},
title = {Finerenone Attenuates Myocardial Fibrosis and Pyroptosis in Rats with Myocardial Infarction.},
journal = {International heart journal},
year = {2026},
doi = {10.1536/ihj.25-278},
note = {PMID: 42219330},
}
TY - JOUR AU - Wen J AU - Ou YC AU - Ke HH AU - Lu YQ AU - Liang LM AU - Li JY TI - Finerenone Attenuates Myocardial Fibrosis and Pyroptosis in Rats with Myocardial Infarction. T2 - International heart journal PY - 2026 DO - 10.1536/ihj.25-278 AN - PMID:42219330 ER -
The mineralocorticoid receptor (MR) plays a pivotal role in cardiovascular diseases, and its overactivation contributes to heart failure (HF) progression. Finerenone (FIN), a novel nonsteroidal MR antagonist (MRA), shows promise in managing postmyocardial infarction (MI) HF. This study investigated the mechanism by which FIN inhibits myocardial remodeling after MI by targeting fibrotic and inflammatory pathways. A rat MI model was established through coronary artery ligation, followed by FIN administration (10 mg/kg/day) for 2 or 4 weeks. Histological (H&E and Masson's staining) and molecular analyses (PCR, Western blot, and immunohistochemistry) revealed elevated collagen deposition and pyroptosis markers in both the infarcted and noninfarcted regions, with greater severity in the infarcted areas. FIN treatment may attenuate fibrosis by suppressing TGF-β signaling and restoring the MMP9/TIMP1 balance, reducing cardiomyocyte pyroptosis, and improving ventricular compliance. FIN demonstrated dual antifibrotic and antipyroptotic effects in both regions post-MI, suggesting a novel therapeutic strategy for HF intervention (Supplemental Figure).