Is there more to aging than mitochondrial DNA and reactive oxygen species?

被引:157
作者
Alexeyev, Mikhail F. [1 ,2 ]
机构
[1] Univ S Alabama, Dept Cell Biol & Neurosci, 307 Univ Blvd,MSB1201, Mobile, AL 36688 USA
[2] Ukrainian Acad Sci, Inst Mol Biol & Genet, UA-252627 Kiev, Ukraine
基金
美国国家卫生研究院;
关键词
antioxidants; lifespan extension; mitochondria; mitochondrial DNA degradation; mitochondrial DNA mutations; mitochondrial DNA repair; mitochondrial theory of aging; oxidative damage; TARGETED PLASTOQUINONE DERIVATIVES; BASE EXCISION-REPAIR; ENDOGENOUS OXIDATIVE DAMAGE; HYDROGEN-PEROXIDE RELEASE; CULTURED SKIN FIBROBLASTS; ZN-SUPEROXIDE-DISMUTASE; LIFE-SPAN; GLUTATHIONE-PEROXIDASE; INTERRUPT EXECUTION; SKELETAL-MUSCLE;
D O I
10.1111/j.1742-4658.2009.07269.x
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
With the aging of the population, we are seeing a global increase in the prevalence of age-related disorders, especially in developed countries. Chronic diseases disproportionately affect the older segment of the population, contributing to disability, a diminished quality of life and an increase in healthcare costs. Increased life expectancy reflects the success of contemporary medicine, which must now respond to the challenges created by this achievement, including the growing burden of chronic illnesses, injuries and disabilities. A well-developed theoretical framework is required to understand the molecular basis of aging. Such a framework is a prerequisite for the development of clinical interventions that will constitute an efficient response to the challenge of age-related health issues. This review critically analyzes the experimental evidence that supports and refutes the Free Radical/Mitochondrial Theory of Aging, which has dominated the field of aging research for almost half a century.
引用
收藏
页码:5768 / 5787
页数:20
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