Mitophagy mechanisms in neuronal physiology and pathology during ageing

被引:9
|
作者
Markaki, Maria [1 ]
Tsagkari, Dikaia [1 ]
Tavernarakis, Nektarios [1 ,2 ]
机构
[1] Fdn Res & Technol Hellas, Inst Mol Biol & Biotechnol, Iraklion 70013, Greece
[2] Univ Crete, Sch Med, Dept Basic Sci, Iraklion 70013, Greece
关键词
Ageing; Energy homeostasis; Mitophagy; Neurodegeneration; Neuronal health; Neuron; MITOCHONDRIAL QUALITY-CONTROL; DAMAGED MITOCHONDRIA; PARKIN TRANSLOCATION; UBIQUITIN CHAINS; IN-VIVO; PINK1; DEGRADATION; AUTOPHAGY; DISEASE; SYSTEM;
D O I
10.1007/s12551-021-00894-7
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
Ageing in diverse species ranging from the simple nematode Caenorhabditis elegans to humans is associated with a marked decrease of neuronal function and increased susceptibility to neurodegeneration. Accumulating findings also indicate that alterations in neuronal functionality with age are associated with a decline in mitochondrial integrity and function. The rate at which a mitochondrial population is refreshed is determined by the coordination of mitochondrial biogenesis with mitophagy, a selective type of autophagy targeting damaged or superfluous mitochondria for degradation. Coupling of these opposing processes is crucial for maintaining cellular energy homeostasis, which eventually contributes to health span. Here, we focus on the role of mitophagy in nervous system function in the context of normal physiology and disease. First, we consider the progress that has been made over the last decade in elucidating the mechanisms that govern and regulate mitophagy, placing emphasis on the PINK1/Parkin-mediated mitophagy. We further discuss the contribution of mitophagy to the maintenance of neuronal homeostasis and health as well as recent findings implicating impaired mitophagy in age-related decline of the nervous system function and consequently in the pathogenesis of neurodegenerative diseases.
引用
收藏
页码:955 / 965
页数:11
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