• Maurizio Forte, Luca D'Ambrosio, Gabriele G Schiattarella, Nadia Salerno, Marco Alfonso Perrone, Francesco S Loffredo, Edoardo Bertero, Kalliopi Pilichou, Girolamo Manno, Valentina Valenti, Luigi Spadafora, Marco Bernardi, Beatrice Simeone, Gianmarco Sarto, Giacomo Frati, Cinzia Perrino, Sebastiano Sciarretta, and Italian Society of Cardiology Working Group on Cellular and Molecular Biology of the Heart.
• IRCCS Neuromed, Pozzilli, Italy.
• Eur. J. Clin. Invest. 2024 Aug 1; 54 (8): e14199e14199.

BackgroundDefects of mitophagy, the selective form of autophagy for mitochondria, are commonly observed in several cardiovascular diseases and represent the main cause of mitochondrial dysfunction. For this reason, mitophagy has emerged as a novel and potential therapeutic target.MethodsIn this review, we discuss current evidence about the biological significance of mitophagy in relevant preclinical models of cardiac and vascular diseases, such as heart failure, ischemia/reperfusion injury, metabolic cardiomyopathy and atherosclerosis.ResultsMultiple studies have shown that cardiac and vascular mitophagy is an adaptive mechanism in response to stress, contributing to cardiovascular homeostasis. Mitophagy defects lead to cell death, ultimately impairing cardiac and vascular function, whereas restoration of mitophagy by specific compounds delays disease progression.ConclusionsDespite previous efforts, the molecular mechanisms underlying mitophagy activation in response to stress are not fully characterized. A comprehensive understanding of different forms of mitophagy active in the cardiovascular system is extremely important for the development of new drugs targeting this process. Human studies evaluating mitophagy abnormalities in patients at high cardiovascular risk also represent a future challenge.© 2024 The Authors. European Journal of Clinical Investigation published by John Wiley & Sons Ltd on behalf of Stichting European Society for Clinical Investigation Journal Foundation.

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