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首页> 外文期刊>Journal of Cachexia, Sarcopenia and Muscle >Redox homeostasis and age-related deficits in neuromuscular integrity and function
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Redox homeostasis and age-related deficits in neuromuscular integrity and function

机译：氧化还原稳态和神经肌肉完整性和功能的年龄相关缺陷

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Abstract Skeletal muscle is a major site of metabolic activity and is the most abundant tissue in the human body. Age-related muscle atrophy (sarcopenia) and weakness, characterized by progressive loss of lean muscle mass and function, is a major contributor to morbidity and has a profound effect on the quality of life of older people. With a continuously growing older population (estimated 2 billion of people aged >60 by 2050), demand for medical and social care due to functional deficits, associated with neuromuscular ageing, will inevitably increase. Despite the importance of this ?￠????epidemic?￠???? problem, the primary biochemical and molecular mechanisms underlying age-related deficits in neuromuscular integrity and function have not been fully determined. Skeletal muscle generates reactive oxygen and nitrogen species (RONS) from a variety of subcellular sources, and age-associated oxidative damage has been suggested to be a major factor contributing to the initiation and progression of muscle atrophy inherent with ageing. RONS can modulate a variety of intracellular signal transduction processes, and disruption of these events over time due to altered redox control has been proposed as an underlying mechanism of ageing. The role of oxidants in ageing has been extensively examined in different model organisms that have undergone genetic manipulations with inconsistent findings. Transgenic and knockout rodent studies have provided insight into the function of RONS regulatory systems in neuromuscular ageing. This review summarizes almost 30 years of research in the field of redox homeostasis and muscle ageing, providing a detailed discussion of the experimental approaches that have been undertaken in murine models to examine the role of redox regulation in age-related muscle atrophy and weakness.
机译：摘要骨骼肌是代谢活动的主要部位，是人体中最丰富的组织。与年龄相关的肌肉萎缩（肌肉减少症）和无力，以瘦肌肉质量和功能的逐渐丧失为特征，是发病率的主要贡献因素，对老年人的生活质量产生深远影响。随着老年人口的不断增长（到2050年，预计有20亿年龄在60岁以上的人口），由于与神经肌肉老化相关的功能缺陷，对医疗和社会护理的需求将不可避免地增加。尽管这种流行病很重要问题是，尚未完全确定与年龄有关的神经肌肉完整性和功能缺陷的主要生化和分子机制。骨骼肌从多种亚细胞来源产生活性氧和氮（RONS），并且与年龄相关的氧化损伤被认为是导致衰老所固有的肌肉萎缩的发生和发展的主要因素。 RONS可以调节多种细胞内信号转导过程，并且由于氧化还原控制的改变而导致的这些事件随时间的破坏已经被提出作为衰老的潜在机制。氧化剂在衰老中的作用已在经过遗传操作且结果不一致的不同模型生物中进行了广泛研究。转基因和基因敲除啮齿类动物研究为RONS调节系统在神经肌肉衰老中的功能提供了见识。这篇综述总结了氧化还原稳态和肌肉老化领域近30年的研究，详细讨论了在鼠模型中研究氧化还原调节在与年龄有关的肌肉萎缩和衰弱中的作用的实验方法。

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