Xu Hongyang, Brown Jacob L, Bhaskaran Shylesh, Van Remmen Holly
Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, United States.
Aging and Metabolism Research Program, Oklahoma Medical Research Foundation, Oklahoma City, OK, 73104, United States; Oklahoma City VA Medical Center, Oklahoma City, OK, 73104, United States.
Free Radic Biol Med. 2025 Feb 1;227:446-458. doi: 10.1016/j.freeradbiomed.2024.11.046. Epub 2024 Nov 28.
One of the most critical factors impacting healthspan in the elderly is the loss of muscle mass and function, clinically referred to as sarcopenia. Muscle atrophy and weakness lead to loss of mobility, increased risk of injury, metabolic changes and loss of independence. Thus, defining the underlying mechanisms of sarcopenia is imperative to enable the development of effective interventions to preserve muscle function and quality in the elderly and improve healthspan. Over the past few decades, understanding the roles of mitochondrial dysfunction and oxidative stress has been a major focus of studies seeking to reveal critical molecular pathways impacted during aging. In this review, we will highlight how oxidative stress might contribute to sarcopenia by discussing the impact of oxidative stress on the loss of innervation and alteration in the neuromuscular junction (NMJ), on muscle mitochondrial function and atrophy pathways, and finally on muscle contractile function.
影响老年人健康寿命的最关键因素之一是肌肉质量和功能的丧失,临床上称为肌肉减少症。肌肉萎缩和无力会导致行动能力丧失、受伤风险增加、代谢变化以及失去独立性。因此,明确肌肉减少症的潜在机制对于开发有效的干预措施至关重要,这些干预措施旨在维持老年人的肌肉功能和质量并改善健康寿命。在过去几十年中,了解线粒体功能障碍和氧化应激的作用一直是旨在揭示衰老过程中受影响的关键分子途径的研究重点。在这篇综述中,我们将通过讨论氧化应激对神经支配丧失和神经肌肉接头(NMJ)改变、对肌肉线粒体功能和萎缩途径以及最终对肌肉收缩功能的影响,来强调氧化应激可能如何导致肌肉减少症。