Mitophagy in cardiovascular diseases: mechanisms and potential therapies

Le résumé fourni par la source

Mitophagy, the selective autophagic degradation of mitochondria, is a critical process for preserving mitochondrial quality and cellular homeostasis in the cardiovascular system. This review systematically outlines the principal molecular mechanisms underlying mitophagy, focusing on the PTEN-induced putative kinase 1 (PINK1)-Parkin pathway and receptor-mediated pathways involving proteins such as BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3) and FUN14 domain-containing protein 1 (FUNDC1). In various cardiovascular diseases, mitophagy is complex and context dependent. When properly regulated, it exerts a protective role by clearing damaged mitochondria, mitigating oxidative stress, and suppressing inflammatory responses. However, the dysregulation of mitophagy—whether it is insufficient or excessive—can contribute to the exacerbation of disease progression. The therapeutic potential of modulating mitophagy through pharmacological agents, genetic interventions, and lifestyle changes is also examined. However, major challenges remain, including the dualistic nature of mitophagy outcomes, the lack of tissue-specific regulators, and the scarcity of clinically applicable modulators. Advancing our understanding of the multi-level regulatory networks governing mitophagy will be essential for developing targeted therapies to combat cardiovascular diseases (CVDs).

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.