Chromatin modifications: The driving force of senescence and aging?

被引:43
作者
DiMauro, Teresa [1 ]
David, Gregory [1 ,2 ]
机构
[1] NYU Langone Med Ctr, Dept Pharmacol, New York, NY 10016 USA
[2] NYU Langone Med Ctr, NYU Canc Inst, New York, NY 10016 USA
来源
AGING-US | 2009年 / 1卷 / 02期
关键词
chromatin; histone; senescence; heterochromatin; methylation; nuclear organization; HUTCHINSON-GILFORD-PROGERIA; CELLULAR SENESCENCE; LAMIN-A; TELOMERE LENGTH; DNA METHYLTRANSFERASES; TUMOR-SUPPRESSOR; MAMMALIAN-CELLS; LIFE-SPAN; HISTONE METHYLTRANSFERASES; HETEROCHROMATIN FORMATION;
D O I
10.18632/aging.100023
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
An emerging field of investigation in the search for treatment of human disease is the modulation of chromatin modifications. Chromatin modifications impart virtually all processes occurring in the mammalian nucleus, from regulation of transcription to genomic stability and nuclear high order organization. It has been well recognized that, as the mammalian cell ages, its chromatin structure evolves, both at a global level and at specific loci. While these observations are mostly correlative, recent technical developments allowing loss-of-function experiments and genome-wide approaches have permitted the identification of a causal relationship between specific changes in chromatin structure and the aging phenotype. Here we review the evidence pointing to the modulation of chromatin structure as a potential driving force of cellular aging in mammals.
引用
收藏
页码:182 / 190
页数:9
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