粒体自噬
神经退行性变
神经保护
线粒体
神经科学
生物
自噬
人口
医学
老化
生物信息学
细胞生物学
遗传学
疾病
病理
细胞凋亡
环境卫生
作者
Guofeng Lou,Konstantinos Palikaras,Sofie Lautrup,Morten Scheibye‐Knudsen,Nektarios Tavernarakis,Evandro Fei Fang
标识
DOI:10.1016/j.molmed.2019.07.002
摘要
Neurodegenerative diseases are strongly age-related and currently cannot be cured, with a surge of patient numbers in the coming decades in view of the emerging worldwide ageing population, bringing healthcare and socioeconomic challenges. Effective therapies are urgently needed, and are dependent on new aetiological mechanisms. In neurons, efficient clearance of damaged mitochondria, through the highly evolutionary conserved cellular process termed mitophagy, plays a fundamental role in mitochondrial and metabolic homeostasis, energy supply, neuronal survival, and health. Conversely, defective mitophagy leads to accumulation of damaged mitochondria and cellular dysfunction, contributing to ageing and age-predisposed neurodegeneration. Here, we discuss the contribution of defective mitophagy in these diseases, and underlying molecular mechanisms, and highlight novel therapeutics based on new discovered mitophagy-inducing strategies.
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