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}
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.