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氧化应激、端粒和细胞衰老:哪些非药物干预措施可能打破这种联系?

Oxidative stress, telomeres and cellular senescence: What non-drug interventions might break the link?

机构信息

The Cellular Senescence and Pathophysiology Group, Cardiff Metropolitan University, Llandaff Campus, Western Avenue, Cardiff, CF5 2YB, United Kingdom.

出版信息

Free Radic Biol Med. 2020 Apr;150:87-95. doi: 10.1016/j.freeradbiomed.2020.02.008. Epub 2020 Feb 13.

Abstract

Telomeres are higher order structures that cap and protect chromosome ends. Telomeric DNA naturally shortens during somatic cell division and as a result of oxidative stress. Excessive shortening disrupts the integrity of the telomere, causing cellular senescence, one of the hallmarks of organismal ageing. The accumulation of senescent cells with ageing contributes to the loss of tissue homeostasis and the development of age-related pathologies. Hence, counteracting telomere shortening may be one relevant approach to develop strategies for healthier ageing. In this review I present the case for the existence of a link between oxidative stress, accelerated telomere shortening and cellular senescence. I also examine findings from human observational studies exploring associations between telomere length and oxidative stress-related parameters. Finally, I discuss results from randomised control trials testing the impact of non-pharmacological lifestyle interventions on the maintenance of telomere length, considering the potential mechanisms that might be involved.

摘要

端粒是一种高级结构,能够覆盖和保护染色体末端。端粒 DNA 在体细胞分裂过程中以及由于氧化应激自然缩短。过度缩短会破坏端粒的完整性,导致细胞衰老,这是生物体衰老的标志之一。随着年龄的增长,衰老细胞的积累导致组织内稳态的丧失和与年龄相关的病理的发展。因此,对抗端粒缩短可能是开发更健康衰老策略的一种相关方法。在这篇综述中,我提出了氧化应激、加速端粒缩短和细胞衰老之间存在联系的观点。我还研究了人类观察性研究中探索端粒长度与氧化应激相关参数之间关系的发现。最后,我讨论了随机对照试验的结果,这些试验测试了非药物生活方式干预对端粒长度维持的影响,同时考虑了可能涉及的潜在机制。

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