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).