DNA damage related crosstalk between the nucleus and mitochondria

被引：120

作者：

Saki, Mohammad ^{[1
]}

Prakash, Aishwarya ^{[1
]}

机构：

[1] Univ S Alabama, Mitchell Canc Inst, 1660 Springhill Ave, Mobile, AL 36604 USA

来源：

FREE RADICAL BIOLOGY AND MEDICINE | 2017年 / 107卷

基金：

美国国家卫生研究院;

关键词：

Reactive oxygen species; Mitochondrial DNA damage; Mitochondrial DNA repair; Mito-nuclear signaling; Oxidative phosphorylation; Mitochondrial dysfunction; REDOX signaling; BASE-EXCISION-REPAIR; UNFOLDED PROTEIN RESPONSE; STRAND BREAK REPAIR; NITRIC-OXIDE; POLYMERASE-GAMMA; MAMMALIAN-CELLS; MISMATCH-REPAIR; SACCHAROMYCES-CEREVISIAE; OXIDATIVE STRESS; GENE-EXPRESSION;

D O I：

10.1016/j.freeradbiomed.2016.11.050

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 electron transport chain is the primary pathway by which a cell generates energy in the form of ATP. Byproducts of this process produce reactive oxygen species that can cause damage to mitochondrial DNA. If not properly repaired, the accumulation of DNA damage can lead to mitochondrial dysfunction linked to several human disorders including neurodegenerative diseases and cancer. Mitochondria are able to combat oxidative DNA damage via repair mechanisms that are analogous to those found in the nucleus. Of the repair pathways currently reported in the mitochondria, the base excision repair pathway is the most comprehensively described. Proteins that are involved with the maintenance of mtDNA are encoded by nuclear genes and translocate to the mitochondria making signaling between the nucleus and mitochondria imperative. In this review, we discuss the current understanding of mitochondrial DNA repair mechanisms and also highlight the sensors and signaling pathways that mediate crosstalk between the nucleus and mitochondria in the event of mitochondrial stress.

引用

页码：216 / 227

页数：12

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