Reflections on telomere dynamics and ageing-related diseases in humans.
Reflections on telomere dynamics and ageing-related diseases in humans.
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对人类端粒动力学和与老年相关疾病的反思。
DOI：
10.1098/rstb.2016.0436
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发表时间：
2018-03-05
期刊：
影响因子：
--
通讯作者：
Shay JW
中科院分区：
文献类型：
--
作者：
Aviv A;Shay JW
流行病学研究主要依赖于白细胞端粒长度（TL）的测量，这反映了其他体细胞的端粒长度。白细胞 TL (LTL) 在个体之间表现出巨大的差异——这种现象已经在新生儿中观察到。它具有高度遗传性，女性的寿命比男性长，非洲血统的个体比欧洲血统的个体长。年长男性怀下的后代的 LTL 也更长。传统观点将 LTL 视为人类衰老的被动生物标志物。然而，新的证据表明，选择性进化力量和 TL 之间的动态相互作用可能会导致特定健康结果的权衡。从生物学角度来看，TL在与衰老相关的人类疾病中可能会发挥积极作用，因为短端粒会增加与细胞增殖受限和组织退化相关的一类疾病的风险，包括心血管疾病，而长端粒会增加另一类与增殖生长增加相关的疾病的风险，包括主要癌症。为了了解端粒生物学在衰老相关疾病中的作用，有必要将端粒研究扩展到新生儿和儿童，并进一步深入了解由于血统和地理位置而导致 TL 变异的根本原因。本文是主题“了解端粒动力学的多样性”的一部分。
Epidemiological studies have principally relied on measurements of telomere length (TL) in leucocytes, which reflects TL in other somatic cells. Leucocyte TL (LTL) displays vast variation across individuals—a phenomenon already observed in newborns. It is highly heritable, longer in females than males and in individuals of African ancestry than European ancestry. LTL is also longer in offspring conceived by older men. The traditional view regards LTL as a passive biomarker of human ageing. However, new evidence suggests that a dynamic interplay between selective evolutionary forces and TL might result in trade-offs for specific health outcomes. From a biological perspective, an active role of TL in ageing-related human diseases could occur because short telomeres increase the risk of a category of diseases related to restricted cell proliferation and tissue degeneration, including cardiovascular disease, whereas long telomeres increase the risk of another category of diseases related to increased proliferative growth, including major cancers. To understand the role of telomere biology in ageing-related diseases, it is essential to expand telomere research to newborns and children and seek further insight into the underlying causes of the variation in TL due to ancestry and geographical location. This article is part of the theme issue ‘Understanding diversity in telomere dynamics’.
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