Cellular and molecular mechanisms of mitochondrial function

被引:612
作者
Osellame, Laura D. [1 ,3 ]
Blacker, Thomas S. [1 ,2 ]
Duchen, Michael R. [1 ,3 ]
机构
[1] UCL, Dept Cell & Dev Biol, London WC1E 6BT, England
[2] UCL, Dept Phys & Astron, London WC1E 6BT, England
[3] UCL, UK Parkinsons Dis Consortium, Inst Neurol, London WC1N 3BG, England
基金
英国惠康基金; 英国医学研究理事会;
关键词
mitochondria; oxidative phosphorylation; apoptosis; intracellular calcium; mitochondrial fission; STRESS-INDUCED APOPTOSIS; CYTOCHROME-C RELEASE; CALCIUM UNIPORTER; MAMMALIAN-CELLS; PERMEABILITY TRANSITION; EMBRYONIC-DEVELOPMENT; PEROXISOMAL FISSION; INSULIN-SECRETION; BH3-ONLY PROTEINS; OLIGOMERIZES BAK;
D O I
10.1016/j.beem.2012.05.003
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Mitochondria are membrane bound organelles present in almost all eukaryotic cells. Responsible for orchestrating cellular energy production, they are central to the maintenance of life and the gatekeepers of cell death. Thought to have originated from symbiotic ancestors, they carry a residual genome as mtDNA encoding 13 proteins essential for respiratory chain function. Mitochondria comprise an inner and outer membrane that separate and maintain the aqueous regions, the intermembrane space and the matrix. Mitochondria contribute to many processes central to cellular function and dysfunction including calcium signalling, cell growth and differentiation, cell cycle control and cell death. Mitochondrial shape and positioning in cells is crucial and is tightly regulated by processes of fission and fusion, biogenesis and autophagy, ensuring a relatively constant mitochondrial population. Mitochondrial dysfunction is implicated in metabolic and age related disorders, neurodegenerative diseases and ischemic injury in heart and brain. (C) 2012 Elsevier Ltd. All rights reserved.
引用
收藏
页码:711 / 723
页数:13
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