Autophagy -Regulated Myocardial Fibrosis: From Mechanistic Exploration to Therapeutic Prospects

Background: Cardiovascular diseases (CVDs) represent a leading cause of global mortality. Myocardial fibrosis (MF), a common pathological hallmark in CVDs, signifies disease progression to severe stages. Its pathogenesis is highly complex, with autophagy playing a pivotal regulatory role. Methods: This narrative review synthesizes and critically evaluates the current literature to elucidate the interplay between MF and autophagy. The focus lies on systematically examining the molecular mechanisms and key signaling pathways involved in autophagy-mediated regulation of MF. Review Content: We systematically examine key molecular pathways and components through which autophagy regulates MF, including mitophagy, the NLRP3 inflammasome, FOXO signaling, the ULK1 complex, the mTOR pathway, and TGF-β signaling. These pathways collectively influence fibroblast activation, collagen metabolism, and overall cardiac extracellular matrix remodeling. Conclusions: Autophagy serves as a crucial modulator of myocardial fibrosis through multiple interconnected molecular pathways. Targeting specific nodes within the autophagic process holds significant therapeutic promise for mitigating MF and slowing CVD progression. This review consolidates current understanding and highlights novel insights, underscoring the need for further research to translate these mechanisms into effective clinical interventions.