Mitochondria, autophagy and age-associated neurodegenerative diseases: New insights into a complex interplay

被引:87
作者
Lionaki, Eirini [1 ]
Markaki, Maria [1 ]
Palikaras, Konstantinos [1 ,2 ]
Tavernarakis, Nektarios [1 ,3 ]
机构
[1] Fdn Res & Technol Hellas, Inst Mol Biol & Biotechnol, Iraklion, Crete, Greece
[2] Univ Crete, Dept Biol, Iraklion, Crete, Greece
[3] Univ Crete, Fac Med, Dept Basic Sci, Iraklion 70013, Crete, Greece
来源
BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS | 2015年 / 1847卷 / 11期
基金
欧洲研究理事会;
关键词
Energy homeostasis; Mitophagy; PINK1; Parkin; Neurodegenerative diseases; Stress response; OXIDATIVE STRESS; CELL-DEATH; DAMAGED MITOCHONDRIA; SELECTIVE AUTOPHAGY; HUNTINGTONS-DISEASE; QUALITY-CONTROL; MITOFUSIN; ENDOPLASMIC-RETICULUM; PARKIN TRANSLOCATION; MUTANT HUNTINGTIN;
D O I
10.1016/j.bbabio.2015.04.010
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
Mitochondria represent the major bioenergetic hub coordinating cellular and organismal homeostasis. The underlying causes of many pathologies tormenting humans converge on impaired mitochondrial maintenance. Mitochondria-specific autophagy (mitophagy), a cellular catabolic process targeting mitochondria, holds a prominent role in mitochondrial quality control. In addition to core autophagic machinery components, mitophagy exploits a variety of molecules that identify damaged or superfluous mitochondria and mediate their elimination. Signaling pathways integrating environmental and genetic stimuli interact with key mitophagy effectors to activate cellular stress response mechanisms, ultimately modulating health and lifespan. Here, we review the signaling cascades and molecular mechanisms that govern the process of mitophagy and discuss their involvement in ageing and neurodegeneration. This article is part of a Special Issue entitled: Mitochondrial Dysfunction in Aging. (c) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:1412 / 1423
页数:12
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