Cell intrinsic and extrinsic mechanisms of stem cell aging depend on telomere status

被引:22
|
作者
Song, Zhangfa [1 ,2 ]
Ju, Zhenyu [1 ,2 ,3 ,4 ]
Rudolph, K. Lenhard [1 ,2 ]
机构
[1] Univ Ulm, Inst Mol Med, D-89081 Ulm, Germany
[2] Univ Ulm, Max Planck Res Grp Stem Cell Aging, D-89081 Ulm, Germany
[3] Chinese Acad Med Sci, Inst Lab Anim Sci, Beijing, Peoples R China
[4] Chinese Acad Med Sci, Max Planck Partner Grp Stem Cell Aging, Beijing, Peoples R China
关键词
Telomere; Stem cell; Aging; ATM-DEFICIENT MICE; BONE-MARROW-TRANSPLANTATION; GENOME-WIDE ASSOCIATION; MURINE HEMATOPOIETIC STEM; AGE-RELATED-CHANGES; LIFE-SPAN; DNA-DAMAGE; ATAXIA-TELANGIECTASIA; MISMATCH REPAIR; DYSFUNCTIONAL TELOMERES;
D O I
10.1016/j.exger.2008.06.009
中图分类号
R592 [老年病学]; C [社会科学总论];
学科分类号
03 ; 0303 ; 100203 ;
摘要
The function of adult stem cells declines during aging and chronic diseases. An understanding of the molecular mechanisms underlying these processes will help to identify targets for future therapies in order to improve regenerative reserve and organ maintenance. Telomere shortening represents a cell intrinsic mechanism inducing DNA damage in aging cells. Current studies in telomerase knockout mice have shown that telomere dysfunction induces cell intrinsic checkpoints and environmental alteration that limit stem cell function. While these phenotypes differ from wild-type mice with long telomere reserves, they appear to be relevant for human aging, which is associated with an accumulation of telomere dysfunction and DNA damage. (c) 2008 Elsevier Inc. All rights reserved.
引用
收藏
页码:75 / 82
页数:8
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