Restoration of mitochondrial function in cells with complex I deficiency

被引:9
|
作者
Bai, YD [1 ]
Park, JS [1 ]
Deng, JH [1 ]
Li, YF [1 ]
Hu, PQ [1 ]
机构
[1] Univ Texas, Hlth Sci Ctr, Dept Cellular & Struct Biol, San Antonio, TX 78229 USA
来源
ROLE OF THE MITOCHONDRIA IN HUMAN AGING AND DISEASE: FROM GENES TO CELL SIGNALING | 2005年 / 1042卷
关键词
complex I deficiency; mtDNA mutation; restoration; revertant; NDI1;
D O I
10.1196/annals.1338.003
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
The mammalian mitochondrial NADH dehydrogenase (complex 1) is the major entry point for the electron transport chain. It is the largest and most complicated respiratory complex consisting of at least 46 subunits, 7 of which are encoded by mitochondrial DNA (mtDNA). Deficiency in complex I function has been associated with various human diseases including neurodegenerative diseases and the aging process. To explore ways to restore mitochondrial function in complex I-deficient cells, various cell models with mutations in genes encoding subunits for complex I have been established. In this paper, we discuss various approaches to recover mitochondrial activity, the complex I activity in particular, in cultured cells.
引用
收藏
页码:25 / 35
页数:11
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