The mitochondrial genome in aging and senescence

被引:57
作者
Lauri, Andrea [1 ]
Pompilio, Giulio [1 ]
Capogrossi, Maurizio C. [2 ]
机构
[1] IRCCS, CCM, Lab Biol Vasc & Med Rigenerat, Milan, Italy
[2] IRCCS, IDI, Lab Patol Vasc, Milan, Italy
关键词
Aging; Senescence; Mitochondria; mtDNA; ROS; Molecular mechanisms; TELOMERASE REVERSE-TRANSCRIPTASE; CYTOCHROME-C-OXIDASE; P53; TUMOR-SUPPRESSOR; MAXIMUM LIFE-SPAN; DNA-DAMAGE; OXIDATIVE STRESS; POINT MUTATIONS; CELLULAR SENESCENCE; GENE-EXPRESSION; REPAIR CAPACITY;
D O I
10.1016/j.arr.2014.07.001
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Aging is characterized by a progressive decline in organism functions due to the impairment of all organs. The deterioration of both proliferative tissues in liver, skin and the vascular system, as well as of largely post-mitotic organs, such as the heart and brain could be attributed at least in part to cell senescence. In this review we examine the role of mitochondrial dysfunction and mtDNA mutations in cell aging and senescence. Specifically, we address how p53 and telomerase reverse transcriptase (TERT) activity switch their roles from cytoprotective to detrimental and also examine the role of microRNAs in cell aging. The proposed role of Reactive Oxygen Species (ROS), both as mutating agents and as signalling molecules, underlying these processes is also described. (C) 2014 Elsevier B.V. All rights reserved.
引用
收藏
页码:1 / 15
页数:15
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