DNA damage in telomeres and mitochondria during cellular senescence: is there a connection?
DNA damage in telomeres and mitochondria during cellular senescence: is there a connection?
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DOI：
10.1093/nar/gkm893
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发表时间：
2007
影响因子：
14.9
通讯作者：
von Zglinicki T
中科院分区：
文献类型：
--
作者：
Passos JF;Saretzki G;von Zglinicki T
Cellular senescence is the ultimate and irreversible loss of replicative capacity occurring in primary somatic cell culture. It is triggered as a stereotypic response to unrepaired nuclear DNA damage or to uncapped telomeres. In addition to a direct role of nuclear DNA double-strand breaks as inducer of a DNA damage response, two more subtle types of DNA damage induced by physiological levels of reactive oxygen species (ROS) can have a significant impact on cellular senescence: Firstly, it has been established that telomere shortening, which is the major contributor to telomere uncapping, is stress dependent and largely caused by a telomere-specific DNA single-strand break repair inefficiency. Secondly, mitochondrial DNA (mtDNA) damage is closely interrelated with mitochondrial ROS production, and this might also play a causal role for cellular senescence. Improvement of mitochondrial function results in less telomeric damage and slower telomere shortening, while telomere-dependent growth arrest is associated with increased mitochondrial dysfunction. Moreover, telomerase, the enzyme complex that is known to re-elongate shortened telomeres, also appears to have functions independent of telomeres that protect against oxidative stress. Together, these data suggest a self-amplifying cycle between mitochondrial and telomeric DNA damage during cellular senescence.
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影响因子：
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影响因子：
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作者：
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DOI：
10.1097/00075197-200011000-00009
发表时间：
2000-11-01
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