Finerenone attenuates myocardial injury and enhances vascular repair via regulation of autophagy, apoptosis, and angiogenesis

  • Sci Rep. 2026 Jun 12. doi: 10.1038/s41598-026-52948-z.
Yebao Wang  1 ,  Junyi Zhang  1 ,  Feng Lv  1 ,  Ting Zhang  1 ,  Yafeng Zhou  2  3
Affiliations
  • 1. Department of Cardiology, Suzhou Dushu Lake Hospital, The Fourth Affiliated Hospital of Soochow University, Medical Center of Soochow University, No.9 Chongwen Road, Industrial Zone, Suzhou, 215000, China.
  • 2. Department of Cardiology, Suzhou Dushu Lake Hospital, The Fourth Affiliated Hospital of Soochow University, Medical Center of Soochow University, No.9 Chongwen Road, Industrial Zone, Suzhou, 215000, China. [email protected].
  • 3. Institute for Hypertension, Soochow University, Suzhou, 215000, China. [email protected].
PMID: 42285992 DOI: 10.1038/s41598-026-52948-z
Abstract

Finerenone, a novel non-steroidal Mineralocorticoid Receptor Antagonist, has demonstrated significant efficacy in the management of myocardial infarction (MI). However, its direct cytoprotective effects on cardiomyocytes and vascular endothelial cells remain unclear. This study was performed to evaluate the cardioprotective and vasoprotective effects of finerenone following MI and to elucidate its underlying mechanisms. An in vitro oxygen-glucose deprivation (OGD) model was utilized to mimic ischemic conditions. H9C2 rat cardiomyoblasts and human umbilical vein endothelial cells were employed to assess the protective effects of finerenone. For in vivo assessment, a murine model of MI was established and treated with oral finerenone for 28 consecutive days. Cardioprotective outcomes were evaluated through electrocardiography, echocardiography, serum biochemical markers, histopathological analyses, and protein expression profiling. Finerenone significantly improved the viability of cardiomyocytes and endothelial cells subjected to OGD, reduced autophagosome accumulation by enhancing autophagosome degradation, inhibited Apoptosis, and promoted endothelial cell migration and tube formation capacity. In vivo, finerenone improved cardiac function parameters, reduced serum levels of myocardial enzyme profiles and brain natriuretic peptides, decreased myocardial infarct size, enhanced left ventricular function, and alleviated myocardial inflammation, fibrosis and Apoptosis. Mechanistically, finerenone downregulated the expression of ATG5 and apoptosis-related molecules in myocardial tissue, while enhancing the expression of Ang and VEGF involved in angiogenesis. Finerenone confers significant cardioprotection by inhibiting Autophagy, Apoptosis, and enhancing angiogenesis in both cardiomyocytes and vascular endothelial cells. These findings provide experimental evidence for the clinical utility of finerenone for secondary prevention after MI.

Keywords
Angiogenesis; Autophagy; Cardioprotection; Finerenone; Myocardial infarction; Vascular repair.
Products