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
{"title":"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","authors":"M. Atayik, Erdem Atasever, Şeydanur Turgut, U. Çakatay","doi":"10.2174/0118746098315667240606052523","DOIUrl":null,"url":null,"abstract":"\n\nAging-related alteration of mitochondrial morphology, impairment in metabolic capacity,\nbioenergetics, and biogenesis are closely associated with loss of muscle mass and function. Mitochondrial\nReactive Oxygen Species (ROS) stimulate muscular redox signaling mechanisms.\nBioenergetic integrity of mitochondria and redox signaling dynamics deteriorates in aged skeletal\nmuscle. Mitochondrial bioenergetic impairment leads to excessive ROS levels and induces the generation\nof defective mitochondria. Higher ROS levels may induce senescence or apoptosis. It is\nnot a resolved issue that mitochondrial dysfunction is either the sole reason or a consequence of\nmuscle loss (or both). However, Increasing evidence emphasizes that dysregulated mitochondrial\nredox signaling has a central role in age-related muscle loss. Nuclear factor erythroid 2-related factor\n2 (Nrf2) regulates redox signaling pathways with the expression of antioxidant genes. As the\naberrant redox signaling mechanisms in aging skeletal muscle become clearer, new natural and\nsynthetic Nrf2-modulating substances and integrated daily physical activity alternatives are coming\ninto view for preventing muscle loss in the elderly. A comprehensive understanding of the relationship\nbetween redox signaling pathways and age-related sarcopenia can help us to prevent sarcopenia\nand its frailty effects with an optimized exercise program as an innovative non-pharmacological\ntherapeutic approach. A further aspect is necessary to consider both individualized physical\ntraining options and alternative Nrf2 signaling modulators. Ameliorating the redox signaling\nwith physical activity and pharmacological interventions may help to prevent sarcopenia and its\nfrailty effects.\n","PeriodicalId":11008,"journal":{"name":"Current aging science","volume":"93 11","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Aging-associated Aberrant Mitochondrial Redox Signaling, Physical\\nActivity, and Sarcopenia\",\"authors\":\"M. Atayik, Erdem Atasever, Şeydanur Turgut, U. Çakatay\",\"doi\":\"10.2174/0118746098315667240606052523\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"\\n\\nAging-related alteration of mitochondrial morphology, impairment in metabolic capacity,\\nbioenergetics, and biogenesis are closely associated with loss of muscle mass and function. Mitochondrial\\nReactive Oxygen Species (ROS) stimulate muscular redox signaling mechanisms.\\nBioenergetic integrity of mitochondria and redox signaling dynamics deteriorates in aged skeletal\\nmuscle. Mitochondrial bioenergetic impairment leads to excessive ROS levels and induces the generation\\nof defective mitochondria. Higher ROS levels may induce senescence or apoptosis. It is\\nnot a resolved issue that mitochondrial dysfunction is either the sole reason or a consequence of\\nmuscle loss (or both). However, Increasing evidence emphasizes that dysregulated mitochondrial\\nredox signaling has a central role in age-related muscle loss. Nuclear factor erythroid 2-related factor\\n2 (Nrf2) regulates redox signaling pathways with the expression of antioxidant genes. As the\\naberrant redox signaling mechanisms in aging skeletal muscle become clearer, new natural and\\nsynthetic Nrf2-modulating substances and integrated daily physical activity alternatives are coming\\ninto view for preventing muscle loss in the elderly. A comprehensive understanding of the relationship\\nbetween redox signaling pathways and age-related sarcopenia can help us to prevent sarcopenia\\nand its frailty effects with an optimized exercise program as an innovative non-pharmacological\\ntherapeutic approach. A further aspect is necessary to consider both individualized physical\\ntraining options and alternative Nrf2 signaling modulators. Ameliorating the redox signaling\\nwith physical activity and pharmacological interventions may help to prevent sarcopenia and its\\nfrailty effects.\\n\",\"PeriodicalId\":11008,\"journal\":{\"name\":\"Current aging science\",\"volume\":\"93 11\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2024-06-12\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current aging science\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.2174/0118746098315667240606052523\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q3\",\"JCRName\":\"Medicine\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current aging science","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.2174/0118746098315667240606052523","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"Medicine","Score":null,"Total":0}
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.
求助全文
通过发布文献求助,成功后即可免费获取论文全文。 去求助
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
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信