The role of mitochondrial DNA mutation on neurodegenerative diseases

被引：110

作者：

Cha, Moon-Yong ^{[1
]}

Kim, Dong Kyu ^{[1
]}

Mook-Jung, Inhee ^{[1
]}

机构：

[1] Seoul Natl Univ, Coll Med, Dept Biochem & Biomed Sci, Seoul 110799, South Korea

来源：

EXPERIMENTAL AND MOLECULAR MEDICINE | 2015年 / 47卷

关键词：

SPINAL MOTOR-NEURONS; ALZHEIMERS-DISEASE; MOUSE MODEL; OXIDATIVE-PHOSPHORYLATION; ENDOPLASMIC-RETICULUM; REPAIR ENZYMES; AMYLOID-BETA; NITRIC-OXIDE; DAMAGE; INFLAMMASOME;

D O I：

10.1038/emm.2014.122

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Many researchers have reported that oxidative damage to mitochondrial DNA (mtDNA) is increased in several age-related disorders. Damage to mitochondrial constituents and mtDNA can generate additional mitochondrial dysfunction that may result in greater reactive oxygen species production, triggering a circular chain of events. However, the mechanisms underlying this vicious cycle have yet to be fully investigated. In this review, we summarize the relationship of oxidative stress-induced mitochondrial dysfunction with mtDNA mutation in neurodegenerative disorders.

引用

页码：e150 / e150

页数：8

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