Mitophagy and Neuroprotection

被引:338
作者
Lou, Guofeng [1 ,2 ]
Palikaras, Konstantinos [3 ,4 ]
Lautrup, Sofie [1 ,2 ]
Scheibye-Knudsen, Morten [5 ]
Tavernarakis, Nektarios [3 ,4 ]
Fang, Evandro F. [1 ,2 ,6 ]
机构
[1] Univ Oslo, Dept Clin Mol Biol, N-1478 Lorenskog, Norway
[2] Akershus Univ Hosp, N-1478 Lorenskog, Norway
[3] Fdn Res & Technol Hellas, Inst Mol Biol & Biotechnol, Iraklion, Greece
[4] Univ Crete, Dept Basic Sci, Fac Med, Iraklion 70013, Crete, Greece
[5] Univ Copenhagen, Dept Cellular & Mol Med, Ctr Hlth Aging, Copenhagen, Denmark
[6] Norwegian Ctr Hlth Ageing NO Age, Oslo, Norway
基金
欧洲研究理事会;
关键词
MITOCHONDRIAL DYSFUNCTION; LIFE-SPAN; MEDIATES MITOPHAGY; INDUCED AUTOPHAGY; OXIDATIVE STRESS; UP-REGULATION; PARKIN; PROTEIN; DEGRADATION; DISEASE;
D O I
10.1016/j.molmed.2019.07.002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
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.
引用
收藏
页码:8 / 20
页数:13
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