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Quantitative assessment of markers for cell senescence.细胞衰老标志物的定量评估。
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Mitochondrial dysfunction accounts for the stochastic heterogeneity in telomere-dependent senescence.线粒体功能障碍导致了端粒依赖性衰老中的随机异质性。
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Stochastic variation in telomere shortening rate causes heterogeneity of human fibroblast replicative life span.端粒缩短速率的随机变化导致人类成纤维细胞复制寿命的异质性。
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A stochastic model of cell replicative senescence based on telomere shortening, oxidative stress, and somatic mutations in nuclear and mitochondrial DNA.基于端粒缩短、氧化应激以及核DNA和线粒体DNA体细胞突变的细胞复制性衰老随机模型。
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Telomere states and cell fates.端粒状态与细胞命运。
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A reassessment of the telomere hypothesis of senescence.衰老端粒假说的重新评估。
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Reconstitution of telomerase activity in normal human cells leads to elongation of telomeres and extended replicative life span.在正常人细胞中重建端粒酶活性会导致端粒延长和复制寿命延长。
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端粒和端粒酶:细胞衰老的承诺理论再探。

Telomeres and telomerase: the commitment theory of cellular ageing revisited.

机构信息

Australian Academy of Science, Canberra, Australia.

出版信息

Sci Prog. 2012;95(Pt 2):199-205. doi: 10.3184/003685012X13361526995348.

DOI:10.3184/003685012X13361526995348
PMID:22893980
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10365536/
Abstract

It is not always realised that separate fibroblast populations of the same strain have very different lifespans, that is, over a million-fold range. This is best documented for human strains WI-38 and MRC-5. There is evidence that it is the molecular clock of telomere shortening which determines the growth potential of these cells. However, if a clock is set and runs its course one would expect parallel cultures to have similar lifespans. The commitment theory of fibroblast ageing proposes that commitment occurs during early cell divisions with a given probability and after that there is then a constant number of divisions until growth ceases. This constant number could be determined by the gradual loss of telomeres. The stochastic feature of the theory is the probability of the loss of the last uncommitted cells or the youngest committed cells. These cells have the longest lifespan and will give rise to the final population.

摘要

人们并不总是意识到同一株的不同成纤维细胞群体具有非常不同的寿命,即相差一百万倍。这在 WI-38 和 MRC-5 这两个人类株系中得到了最好的证明。有证据表明,是端粒缩短的分子钟决定了这些细胞的生长潜力。然而,如果设置了一个时钟并让其运行,人们会期望平行培养物具有相似的寿命。成纤维细胞衰老的承诺理论提出,在给定的概率下,在早期细胞分裂中发生承诺,之后直到生长停止,就会有一个固定数量的分裂。这个固定数量可能由端粒的逐渐丢失决定。该理论的随机特征是最后一个未承诺细胞或最年轻的承诺细胞丢失的概率。这些细胞具有最长的寿命,并将产生最终的群体。