Oxidative stress response and Nrf2 signaling in aging.
Oxidative stress response and Nrf2 signaling in aging.
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DOI：
10.1016/j.freeradbiomed.2015.05.036
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发表时间：
2015-11
影响因子：
7.4
通讯作者：
Forman HJ
中科院分区：
文献类型：
--
作者：
Zhang H;Davies KJA;Forman HJ
氧化应激的增加是衰老的一个主要特征，与各种年龄相关的病理有关。在衰老过程中，几种来源的氧化剂产生增加，而抗氧化酶（主要的防线）减少。修复系统，包括受损蛋白质的蛋白酶体降解也下降。重要的是，对氧化应激的适应性反应随着年龄的增长而下降。Nrf2/EpRE信号通路调节许多抗氧化酶和蛋白酶体的基础和诱导表达。Nrf2/EpRE的活性在转录、翻译后和与其他蛋白的相互作用等多个水平上受到调控。本文综述了Nrf2/EpRE功能年龄相关损伤的研究现状，并讨论了Nrf2调控机制随年龄的变化。
Increasing oxidative stress, a major characteristic of aging, has been implicated in variety of age-related pathologies. In aging, oxidant production from several sources is increased while antioxidant enzymes, the primary lines of defense, are decreased. Repair systems, including the proteasomal degradation of damaged proteins also declines. Importantly, the adaptive response to oxidative stress declines with aging. Nrf2/EpRE signaling regulates the basal and inducible expression of many antioxidant enzymes and the proteasome. Nrf2/EpRE activity is regulated at several levels including transcription, post-translation, and interaction with other proteins. This review summarizes current studies on age-related impairment of Nrf2/EpRE function and discusses the change of Nrf2 regulatory mechanisms with aging.