粒体自噬
自噬
线粒体
心肌病
机制(生物学)
医学
帕金
生物信息学
疾病
神经科学
生物
心力衰竭
心脏病学
内科学
细胞生物学
帕金森病
遗传学
细胞凋亡
哲学
认识论
作者
Maurizio Forte,Luca D’Ambrosio,Gabriele G. Schiattarella,Nadia Salerno,Marco Alfonso Perrone,Francesco Loffredo,Edoardo Bertero,Kalliopi Pilichou,Girolamo Manno,Valentina Valenti,Luigi Spadafora,Marco Bernardi,Bruno Simeone,Gianmarco Sarto,Giacomo Frati,Cinzia Perrino,Sebastiano Sciarretta
摘要
Defects 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.In 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.Multiple 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.Despite 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.
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