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Sestrins: Novel antioxidant and AMPK-modulating functions regulated by exercise?

机译:抗氧化和AMPK-modulating Sestrins:小说函数由运动吗?

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摘要

Oxidative stress results from damage to tissues caused by free radicals and is increased by exercise. Peroxiredoxins (PRXs) maintain the cellular reducing environment by scavenging intracellular hydrogen peroxide. It has been recently noted that physical exercise has a positive effect on the PRX system, exerting a protective effect against oxidative stress-induced damage. However, other compounds, such as sestrins (SESNs), a stress-inducible protein family with antioxidant properties, should also be considered in the function of PRXs. SESNs are clearly involved in the regeneration process of PRXs and therefore may also be modulated by physical exercise. In addition, SESNs are clearly involved in TOR, AMPK, p53, FoxO, and PRXs signaling pathways. The aforementioned pathways are implicated in aging processes by inducing an increased resistance to subsequent stress, thus delaying age-related changes, such as sarcopenia and frailty, and consequently promoting longevity. Likewise, exercise also modulates these pathways. In fact, exercise is one of the most important recommended strategies to prevent sarcopenia and frailty, increase longevity, and improve health in the elderly. Loss of SESNs can cause several chronic pathologies, such as fat accumulation, mitochondrial dysfunction, cardiac arrhythmia, and/or muscle degeneration. Accordingly, physical inactivity leads to accumulation of visceral fat and consequently the activation of a network of inflammatory pathways, which promote development of insulin resistance, atherosclerosis, neurodegeneration, and tumor growth. To date, the SESNs-exercise relationship has not been explored. However, this emerging family of stress proteins may be part of the redox-based adaptive response to exercise.
机译:氧化应激的结果损害组织引起的自由基,增加了锻炼。细胞减少环境中清除细胞内过氧化氢。最近指出,体育锻炼有一个插件可以系统上的积极影响,施加了一个抗氧化的作用应激损伤。stress-inducible如sestrins (SESNs)蛋白质家族具有抗氧化特性,还应该考虑的功能插件可以。插件可以再生过程,因此可能体育锻炼也是调制。另外,SESNs显然是参与TOR,FoxO AMPK, p53,插件可以信号通路。上述途径是与衰老过程诱导阻力增加随后的应力,从而延缓与年龄相关变化,如sarcopenia和脆弱因此促进长寿。练习也要调节这些途径。锻炼是最重要的一个建议策略来防止sarcopenia和脆弱,增加寿命,改善健康老人。病态,比如脂肪积累,线粒体功能障碍,心律失常,和/或肌肉退化。缺乏运动导致内脏脂肪的积累因此网络的激活炎症通路,促进发展胰岛素抵抗,动脉粥样硬化,神经衰弱,肿瘤的生长。SESNs-exercise没有关系探索。蛋白质可能redox-based适应性的一部分应对运动。

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