Aging is a process of progressive decline in physiological functions. Cells and tissues in our body are constantly exposed to a variety of endogenous and exogenous assaults that cause, DNA damages. The accumulation of unrepaired/irreparable DNA damages results in a sustained DNA damage checkpoint response and induces cellular senescence, a permanent cell cycle arrest. Studies on human premature aging syndromes have suggested that accumulated damages might lead to exhaustion of resources that are required for replacement of the damaged tissues and thus accelerate aging. In this chapter, we summarize current knowledge on DNA damage repair machinery and evidence supporting the idea that defects in genomic maintenance are behind human premature aging syndromes. We put the emphasis on Hutchinson-Gilford Progeria Syndrome.
KeywordsPremature aging DNA damage Lamin A Progerin Chromatin remodeling Epigenetics
B.L. is an Excellent Young Researcher of National Natural Science Foundation of China (81422016), an awardee of 1000-Young Talents Program (The Organization Department of the Communist Party of China Central Committee), and supported by the Major Research plan of NSFC (91439133). Works in Z.Z.’s laboratory are supported by a NSFC Key Project grant (81330009), a National Key Basic Research Program project (2011CB964700) from Ministry of Science and Technology of China, and a RGC grant (HKU2/CRF/13G) from Hong Kong SAR.
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