肌萎缩
骨骼肌
长寿
医学
适应性反应
生物
平衡
生物信息学
胰岛素抵抗
神经科学
老化
损失函数
葡萄糖稳态
生长细胞
内分泌学
衰老
表型
限制
浪费的
肌肉肥大
发病机制
受体
功能(生物学)
生长激素
肌动蛋白
内科学
激素
再生(生物学)
健康衰老
生理学
心理干预
作者
Matthew J. Johnston,Holly M Brown-Borg
标识
DOI:10.1016/j.arr.2025.102946
摘要
The gap between lifespan and healthspan is increasing globally, resulting in millions of individuals spending additional years burdened by frailty or disease. This disparity, paired with the increasingly aged populations of Western nations, poses a palpable predicament to public health and the economy. Deterioration of the skeletal muscle system is a key contributor to illness, loss of independence, and diminishing healthspan. Muscle quality correlates to longevity due to its significant role in metabolic homeostasis and autonomous mobility, reducing instances of adverse events such as falls and fractures. The age-related loss of muscle mass and function is termed sarcopenia, affecting older adults ubiquitously without intervention through regular resistance training. Although clinical manifestations of sarcopenia are well characterized, the molecular mechanisms underlying its pathogenesis remain incompletely understood, limiting the development of targeted, mechanism-based interventions. To identify interventions beyond exercise that delay sarcopenia, it is necessary to identify early onset physiological alterations defining this process. Genetically modified mouse models of accelerated or delayed aging offer valuable insight into the cellular mechanisms that drive or mitigate sarcopenia. The latter is often achieved by disrupting the somatotropic axis, as multiple models exist that either lack growth hormone (GH) production or a functional GH receptor (GHR) paired with a secondary deficiency in insulin like growth factor-1 (IGF-1), which reliably extends lifespan across various species. This review evaluates GH's paradoxical role in muscular maintenance and contrasts the skeletal muscle health of various murine models of aging in effort to better outline the molecular underpinnings of sarcopenia.
科研通智能强力驱动
Strongly Powered by AbleSci AI