Dunn Phoebe L, Logeswaran Dhenugen, Chen Julian J-L
School of Life Sciences, Arizona State University, Tempe, Arizona, USA.
School of Molecular Sciences, Arizona State University, Tempe, Arizona, USA.
Subcell Biochem. 2024;107:1-20. doi: 10.1007/978-3-031-66768-8_1.
The ageing process involves a gradual decline of chromosome integrity throughout an organism's lifespan. Telomeres are protective DNA-protein complexes that cap the ends of linear chromosomes in eukaryotic organisms. Telomeric DNA consists of long stretches of short "TTAGGG" repeats that are conserved across most eukaryotes including humans. Telomeres shorten progressively with each round of DNA replication due to the inability of conventional DNA polymerase to completely replicate the chromosome ends, known as the "end-replication problem". The telomerase enzyme counteracts the telomeric DNA loss by de novo addition of telomeric repeats onto chromosomal ends. Germline and stem cells maintain significant levels of telomerase activity to maintain telomere length and can divide almost indefinitely. However, the differentiation of stem cells accompanies the inactivation of telomerase gene expression, resulting in the progressive shortening of telomeres in somatic cells over successive divisions. Critically short telomeres elicit and sustain a persistent DNA damage response leading to permanent growth arrest of cells known as cellular senescence, a hallmark of cellular ageing. The accumulation of senescent cells in tissues and organs contributes to organismal ageing. Thus, the prevention of telomere shortening is a promising means to delay or even reverse cellular ageing. In this chapter, we summarize potential anti-ageing interventions that mitigate telomere shortening through increasing telomerase level or activity and discuss these strategies' risks, benefits, and future outlooks.
衰老过程涉及生物体整个生命周期中染色体完整性的逐渐下降。端粒是一种保护性的DNA - 蛋白质复合物,位于真核生物线性染色体的末端。端粒DNA由长串短的“TTAGGG”重复序列组成,在包括人类在内的大多数真核生物中都是保守的。由于传统DNA聚合酶无法完全复制染色体末端,即所谓的“末端复制问题”,端粒在每一轮DNA复制中都会逐渐缩短。端粒酶通过在染色体末端从头添加端粒重复序列来抵消端粒DNA的丢失。生殖细胞和干细胞保持着高水平的端粒酶活性以维持端粒长度,并且几乎可以无限分裂。然而,干细胞的分化伴随着端粒酶基因表达的失活,导致体细胞在连续分裂过程中端粒逐渐缩短。极短的端粒引发并维持持续的DNA损伤反应,导致细胞永久性生长停滞,即细胞衰老,这是细胞衰老的一个标志。衰老细胞在组织和器官中的积累促成了机体的衰老。因此,预防端粒缩短是延缓甚至逆转细胞衰老的一种有前景的方法。在本章中,我们总结了通过提高端粒酶水平或活性来减轻端粒缩短的潜在抗衰老干预措施,并讨论了这些策略的风险、益处和未来展望。