与衰老相关的线粒体氧化还原信号异常、体力活动和肌肉疏松症

Q3 Medicine
M. Atayik, Erdem Atasever, Şeydanur Turgut, U. Çakatay
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引用次数: 0

摘要

与衰老有关的线粒体形态改变、代谢能力、生物能和生物生成的损害与肌肉质量和功能的丧失密切相关。线粒体活性氧(ROS)会刺激肌肉氧化还原信号机制。线粒体生物能受损会导致 ROS 水平过高,并诱发缺陷线粒体的产生。较高的 ROS 水平可能会诱发衰老或细胞凋亡。线粒体功能障碍是肌肉损失的唯一原因或后果(或两者兼而有之),这个问题尚未解决。然而,越来越多的证据强调,线粒体氧化还原信号失调在与年龄相关的肌肉衰减中起着核心作用。核因子红细胞 2 相关因子 2(Nrf2)通过抗氧化基因的表达来调节氧化还原信号通路。随着衰老骨骼肌中异常氧化还原信号机制的日益清晰,新的天然和合成 Nrf2 调节物质以及综合日常体育锻炼替代品正逐渐被用于预防老年人肌肉流失。全面了解氧化还原信号通路与老年性肌肉疏松症之间的关系,有助于我们通过优化运动计划这种创新的非药物治疗方法来预防肌肉疏松症及其对身体虚弱的影响。此外,还需要考虑个性化的体育训练方案和替代性的 Nrf2 信号调节剂。通过体育锻炼和药物干预来改善氧化还原信号,可能有助于预防肌肉疏松症及其衰弱效应。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Aging-associated Aberrant Mitochondrial Redox Signaling, Physical Activity, and Sarcopenia
Aging-related alteration of mitochondrial morphology, impairment in metabolic capacity, bioenergetics, and biogenesis are closely associated with loss of muscle mass and function. Mitochondrial Reactive Oxygen Species (ROS) stimulate muscular redox signaling mechanisms. Bioenergetic integrity of mitochondria and redox signaling dynamics deteriorates in aged skeletal muscle. Mitochondrial bioenergetic impairment leads to excessive ROS levels and induces the generation of defective mitochondria. Higher ROS levels may induce senescence or apoptosis. It is not a resolved issue that mitochondrial dysfunction is either the sole reason or a consequence of muscle loss (or both). However, Increasing evidence emphasizes that dysregulated mitochondrial redox signaling has a central role in age-related muscle loss. Nuclear factor erythroid 2-related factor 2 (Nrf2) regulates redox signaling pathways with the expression of antioxidant genes. As the aberrant redox signaling mechanisms in aging skeletal muscle become clearer, new natural and synthetic Nrf2-modulating substances and integrated daily physical activity alternatives are coming into view for preventing muscle loss in the elderly. A comprehensive understanding of the relationship between redox signaling pathways and age-related sarcopenia can help us to prevent sarcopenia and its frailty effects with an optimized exercise program as an innovative non-pharmacological therapeutic approach. A further aspect is necessary to consider both individualized physical training options and alternative Nrf2 signaling modulators. Ameliorating the redox signaling with physical activity and pharmacological interventions may help to prevent sarcopenia and its frailty effects.
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来源期刊
Current aging science
Current aging science Medicine-Geriatrics and Gerontology
CiteScore
3.90
自引率
0.00%
发文量
40
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