Mitophagy

被引:225
作者
Tolkovsky, Aviva M. [1 ]
机构
[1] Univ Cambridge, Dept Biochem, Cambridge CB2 1QW, England
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH | 2009年 / 1793卷 / 09期
基金
英国惠康基金;
关键词
Autophagy; Mitochondria; LC3; Parkin; Nix; Ulk1; MITOCHONDRIAL PERMEABILITY TRANSITION; CELL-DEATH; AUTOPHAGIC DEGRADATION; ORGANELLE DEGRADATION; OXIDATIVE STRESS; YEAST; FISSION; PROTEIN; FUSION; PINK1;
D O I
10.1016/j.bbamcr.2009.03.002
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
Concurrent mitochondrial elimination and autophagy in many systems has led to the proposal that autophagy is the main mechanism of mitochondrial turnover during development and under pathological conditions. The term mitophagy was coined to describe the selective removal of mitochondria by autophagy but the process itself is still contentious. Three questions are being debated: I) Is there a specific removal of mitochondria, by autophagy or is it non-selective or inadvertent? 2) What are the signals that drive this process? 3) Does removal of mitochondria increase or decrease cell viability? There is a mounting evidence for specific signals in/on mitochondria that drive mitochondrial removal from cells by autophagy. The process itself may be both selective and non-selective. In yeast, surprisingly, mitochondrial elimination occurs more by microautophagy (intracellular pinocytosis by the vacuolar membrane) than macroautophagy (initiated by stand-alone nascent double membrane structures known as autophagosomes). In mammalian cells, macroautophagy seems most prevalent though tools to study microautophagy are not well developed. Whilst lack of mitophagy seems to be deleterious, understanding the interplay between autophagy, mitochondrial performance, and cell pathology is a much-needed area of research. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:1508 / 1515
页数:8
相关论文
共 73 条
[1]   Mitophagy - The life-or-death dichotomy includes yeast [J].
Abeliovich, Hagai .
AUTOPHAGY, 2007, 3 (03) :275-277
[2]   Bax/Bak-dependent release promotes of DDP/TIMM8a promotes Drp1-mediated mitochondrial fission and mitoptosis during programmed cell death [J].
Arnoult, D ;
Rismanchi, N ;
Grodet, A ;
Roberts, RG ;
Seeburg, DP ;
Estaquier, J ;
Sheng, M ;
Blackstone, C .
CURRENT BIOLOGY, 2005, 15 (23) :2112-2118
[3]   CYTOPLASMIC COMPONENTS IN HEPATIC CELL LYSOSOMES [J].
ASHFORD, TP ;
PORTER, KR .
JOURNAL OF CELL BIOLOGY, 1962, 12 (01) :198-&
[4]   Nitric oxide-induced mitochondrial fission is regulated by dynamin-related GTPases in neurons [J].
Barsoum, Mark J. ;
Yuan, Hua ;
Gerencser, Akos A. ;
Liot, Geraldine ;
Kushnareva, Yulia E. ;
Graeber, Simone ;
Kovacs, Imre ;
Lee, Wilson D. ;
Waggoner, Jenna ;
Cui, Jiankun ;
White, Andrew D. ;
Bossy, Blaise ;
Martinou, Jean-Claude ;
Youle, Richard J. ;
Lipton, Stuart A. ;
Ellisman, Mark H. ;
Perkins, Guy A. ;
Bossy-Wetzel, Ella .
EMBO JOURNAL, 2006, 25 (16) :3900-3911
[5]   ULTRASTRUCTURAL-STUDY OF NORMAL DEGENERATION OF INTERSEGMENTAL MUSCLES OF ANTHERAEA-POLYPHEMUS AND MANDUCA-SEXTA (INSECTA, LEPIDOPTERA) WITH PARTICULAR REFERENCE TO CELLULAR AUTOPHAGY [J].
BEAULATION, J ;
LOCKSHIN, RA .
JOURNAL OF MORPHOLOGY, 1977, 154 (01) :39-57
[6]   Mitochondrial fission and fusion dynamics: the long and short of it [J].
Berman, S. B. ;
Pineda, F. J. ;
Hardwick, J. M. .
CELL DEATH AND DIFFERENTIATION, 2008, 15 (07) :1147-1152
[7]   Uth1p:: a yeast mitochondrial protein at the crossroads of stress, degradation and cell death [J].
Camougrand, N ;
Kissová, I ;
Velours, G ;
Manon, S .
FEMS YEAST RESEARCH, 2004, 5 (02) :133-140
[8]   The product of the UTH1 gene, required for Bax-induced cell death in yeast, is involved in the response to rapamycin [J].
Camougrand, N ;
Grelaud-Coq, A ;
Marza, E ;
Priault, M ;
Bessoule, JJ ;
Manon, S .
MOLECULAR MICROBIOLOGY, 2003, 47 (02) :495-506
[9]   Aging and oxidative stress: studies of some genes involved both in aging and in response to oxidative stress [J].
Camougrand, N ;
Rigoulet, M .
RESPIRATION PHYSIOLOGY, 2001, 128 (03) :393-401
[10]   MITOCHONDRIAL MORPHOLOGICAL AND FUNCTIONAL DEFECTS IN YEAST CAUSED BY YME1 ARE SUPPRESSED BY MUTATION OF A 26S PROTEASE SUBUNIT HOMOLOG [J].
CAMPBELL, CL ;
TANAKA, N ;
WHITE, KH ;
THORSNESS, PE .
MOLECULAR BIOLOGY OF THE CELL, 1994, 5 (08) :899-905