氧化应激和端粒DNA损伤。

IF 6.9 2区 生物学 Q1 CELL BIOLOGY
Patricia L Opresko, Samantha L Sanford, Mariarosaria De Rosa
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引用次数: 0

摘要

氧化应激与端粒缩短和端粒功能障碍增加有关,也与许多人类病理有关,包括炎症性疾病和癌症。极短和功能失调的端粒失去了保护染色体末端的能力,从而引发不可逆转的生长停滞,称为衰老或基因组不稳定。端粒对活性氧的损伤高度敏感,在氧化应激条件下,活性氧会增加。这项工作涵盖了端粒DNA氧化损伤通过各种机制改变端粒维持的证据,并描述了在氧化应激条件下保持端粒功能的重要DNA修复途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Oxidative Stress and DNA Damage at Telomeres.

Oxidative stress is associated with increasing telomere shortening and telomere dysfunction, as well as with numerous pathologies in humans, including inflammatory diseases and cancer. Critically short and dysfunctional telomeres lose their ability to protect chromosome ends, which triggers irreversible growth arrest, termed senescence, or genomic instability. Telomeres are highly sensitive to damage from reactive oxygen species, which increase under conditions of oxidative stress. This work covers the evidence that oxidative damage to telomeric DNA alters telomere maintenance by various mechanisms and describes the DNA repair pathways important for preserving telomere function under oxidative stress conditions.

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来源期刊
CiteScore
15.00
自引率
1.40%
发文量
56
审稿时长
3-8 weeks
期刊介绍: Cold Spring Harbor Perspectives in Biology offers a comprehensive platform in the molecular life sciences, featuring reviews that span molecular, cell, and developmental biology, genetics, neuroscience, immunology, cancer biology, and molecular pathology. This online publication provides in-depth insights into various topics, making it a valuable resource for those engaged in diverse aspects of biological research.
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