Mechanisms of mitophagy

被引：2505

作者：

Youle, Richard J. ^{[1
]}

Narendra, Derek P. ^{[1
,2
]}

机构：

[1] NINDS, Biochem Sect, Surg Neurol Branch, NIH, Bethesda, MD 20892 USA

[2] Med Res Council Mitochondrial Biol Unit, Cambridge CB2 2XY, England

来源：

NATURE REVIEWS MOLECULAR CELL BIOLOGY | 2011年 / 12卷 / 01期

关键词：

MITOCHONDRIAL-DNA DELETIONS; PINK1/PARKIN-MEDIATED MITOPHAGY; AUTOPHAGOSOME FORMATION; PARKINSON-DISEASE; PINK1; PROTEIN; NIX; DEGRADATION; MUTATIONS; P62/SQSTM1;

D O I：

10.1038/nrm3028

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Autophagy not only recycles intracellular components to compensate for nutrient deprivation but also selectively eliminates organelles to regulate their number and maintain quality control. Mitophagy, the specific autophagic elimination of mitochondria, has been identified in yeast, mediated by autophagy-related 32 (Atg32), and in mammals during red blood cell differentiation, mediated by NIP3-like protein X (NIX; also known as BNIP3L). Moreover, mitophagy is regulated in many metazoan cell types by parkin and PTEN-induced putative kinase protein 1 (PINK1), and mutations in the genes encoding these proteins have been linked to forms of Parkinson's disease.

引用

页码：9 / 14

页数：6

共 72 条

[1] The proapoptotic factor Nix is coexpressed with Bcl-xL during terminal erythroid differentiation [J].

Aerbajinai, W ;

Giattina, M ;

Lee, YT ;

Raffeld, M ;

Miller, JL .

BLOOD, 2003, 102 (02) :712-717

[2] Phylogenomics of life-or-death switches in multicellular animals: Bcl-2, BH3-only, and BNip families of apoptotic regulators [J].

Aouacheria, A ;

Brunet, F ;

Gouy, M .

MOLECULAR BIOLOGY AND EVOLUTION, 2005, 22 (12) :2395-2416

[3] Autophagosome formation from membrane compartments enriched in phosphatidylinositol 3-phosphate and dynamically connected to the endoplasmic reticulum [J].

Axe, Elizabeth L. ;

Walker, Simon A. ;

Manifava, Maria ;

Chandra, Priya ;

Roderick, H. Llewelyn ;

Habermann, Anja ;

Griffiths, Gareth ;

Ktistakis, Nicholas T. .

JOURNAL OF CELL BIOLOGY, 2008, 182 (04) :685-701

[4] Familial parkinsonism and ophthalmoplegia from a mutation in the mitochondrial DNA helicase twinkle [J].

Baloh, Robert H. ;

Salavaggione, Ezequiel ;

Milbrandt, Jeffrey ;

Pestronk, Alan .

ARCHIVES OF NEUROLOGY, 2007, 64 (07) :998-1000

[5] High levels of mitochondrial DNA deletions in substantia nigra neurons in aging and Parkinson disease [J].

Bender, A ;

Krishnan, KJ ;

Morris, CM ;

Taylor, GA ;

Reeve, AK ;

Perry, RH ;

Jaros, E ;

Hersheson, JS ;

Betts, J ;

Klopstock, T ;

Taylor, RW ;

Turnbull, DM .

NATURE GENETICS, 2006, 38 (05) :515-517

[6] Parkin, a gene implicated in autosomal recessive juvenile parkinsonism, is a candidate tumor suppressor gene on chromosome 6q25-q27 (Publication with Expression of Concern. See vol. 114, 2017) [J].

Cesari, R ;

Martin, ES ;

Calin, GA ;

Pentimalli, F ;

Bichi, R ;

McAdams, H ;

Trapasso, F ;

Drusco, A ;

Shimizu, M ;

Mascillo, V ;

d'Andrilli, G ;

Scambia, G ;

Picchio, MC ;

Alder, H ;

Godwin, AK ;

Croce, CM .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2003, 100 (10) :5956-5961

[7] Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin [J].

Clark, Ira E. ;

Dodson, Mark W. ;

Jiang, Changan ;

Cao, Joseph H. ;

Huh, Jun R. ;

Seol, Jae Hong ;

Yoo, Soon Ji ;

Hay, Bruce A. ;

Guo, Ming .

NATURE, 2006, 441 (7097) :1162-1166

[8] The Role of Parkin in Familial and Sporadic Parkinson's Disease [J].

Dawson, Ted M. ;

Dawson, Valina L. .

MOVEMENT DISORDERS, 2010, 25 (03) :S32-S39

[9] FUNCTIONS OF LYSOSOMES [J].

DEDUVE, C ;

WATTIAUX, R .

ANNUAL REVIEW OF PHYSIOLOGY, 1966, 28 :435-+

[10] The Parkinson's disease genes pink1 and parkin promote mitochondrial fission and/or inhibit fusion in Drosophila [J].

Deng, Hansong ;

Dodson, Mark W. ;

Huang, Haixia ;

Guo, Ming .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2008, 105 (38) :14503-14508

← 1 2 3 4 5 6 7 8 →