Signaling Pathways and Therapeutic Approaches in Post-Myocardial Infarction Fibrosis

Abstract

Myocardial infarction (MI) is a leading cause of myocardial fibrosis, contributing significantly to heart disease morbidity and mortality. Recent advancements have elucidated various signaling pathways and therapeutic strategies targeting myocardial fibrosis following MI. This review summarizes key pathways, including TGF-b1, PI3K/AKT, STAT3, AMPK, Nrf2, NF-kB, NLRP3 inflammasome, Wnt/b-catenin, MAPK, and P53, highlighting their potential in therapeutic interventions in recent years. Drug therapy, protein therapy, gene therapy, physical therapy, cell therapy, and exercise training have all shown promise in mitigating fibrosis through these pathways. Notably, multi-pathway therapeutic strategies offer a comprehensive approach to managing myocardial fibrosis, with the TGF-b1 pathway acting as a central hub in the regulatory network. This review underscores the need for further clinical studies to optimize therapeutic strategies and improve outcomes for patients with myocardial fibrosis following MI.