Gao Yin, Liu Di, Xiao Qixian, Huang Shan, Li Li, Xie Baocheng, Zhou Limin, Qi Yi, Liu Yanzhi
Key Laboratory of Traditional Chinese Medicine for the Prevention and Treatment of Infectious Diseases, Institute of Clinical Medicine, Zhanjiang Central Hospital, Guangdong Medical University, Zhanjiang, 524037, People's Republic of China.
Marine Medical Research Institute of Zhanjiang, School of Ocean and Tropical Medicine, Guangdong Medical University, Zhanjiang, 524023, People's Republic of China.
Clin Interv Aging. 2025 May 23;20:659-684. doi: 10.2147/CIA.S517833. eCollection 2025.
Sarcopenia a progressive and multifactorial musculoskeletal syndrome characterized by loss of muscle mass and function, poses a significant global health challenge, particularly in aging populations. Epidemiological studies reveal that sarcopenia affects approximately 5-10% of the general population, with prevalence rates escalating dramatically after age 60 to reach 10-27% in older adults. This age-associated increase contributes significantly to healthcare burdens by elevating risks of disability, frailty, and mortality. Despite its profound impact, current clinical approaches to sarcopenia remain limited. While resistance exercise and protein supplementation form the cornerstone of management, their efficacy is often constrained by poor long-term adherence and variable individual responses, highlighting the urgent need for more comprehensive and personalized treatment strategies. The pathogenesis of sarcopenia is complex and influenced by various factors, including aging, inflammation, nutritional deficits, physical inactivity, and mitochondrial dysfunction. However, the precise molecular mechanisms underlying this condition are still not fully understood. Recent research has made significant strides in elucidating the intricate mechanisms contributing to sarcopenia, revealing novel insights into its molecular and cellular underpinnings. Notably, emerging evidence points to the pivotal role of mitochondrial dysfunction, altered myokine profiles, and neuromuscular junction degeneration in sarcopenia progression. Additionally, breakthroughs in stem cell therapy, exosome-based treatments, and precision nutrition offer promising avenues for clinical intervention. This review aims to synthesize the latest advancements in sarcopenia research, focusing on the novel contributions to its pathogenesis and treatment strategies. We explore emerging trends such as the role of cellular senescence, epigenetic regulation, and targeted therapeutic interventions that could reshape future approaches to managing sarcopenia. By highlighting recent breakthroughs and cutting-edge research, we hope to advance the understanding of sarcopenia and foster the translation of these findings into effective clinical therapies.
肌肉减少症是一种渐进性、多因素的肌肉骨骼综合征,其特征为肌肉质量和功能丧失,对全球健康构成重大挑战,尤其是在老年人群体中。流行病学研究表明,肌肉减少症影响约5%-10%的普通人群,60岁以后患病率急剧上升,在老年人中达到10%-27%。这种与年龄相关的增加通过增加残疾、虚弱和死亡风险,显著加重了医疗负担。尽管其影响深远,但目前针对肌肉减少症的临床方法仍然有限。虽然抗阻运动和蛋白质补充是管理的基石,但其疗效往往受到长期依从性差和个体反应差异的限制,这凸显了对更全面和个性化治疗策略的迫切需求。肌肉减少症的发病机制复杂,受多种因素影响,包括衰老、炎症、营养缺乏、身体活动不足和线粒体功能障碍。然而,这种疾病的确切分子机制仍未完全了解。最近的研究在阐明导致肌肉减少症的复杂机制方面取得了重大进展,揭示了其分子和细胞基础的新见解。值得注意的是,新出现的证据表明线粒体功能障碍、肌细胞因子谱改变和神经肌肉接头退化在肌肉减少症进展中起关键作用。此外,干细胞治疗、基于外泌体的治疗和精准营养方面的突破为临床干预提供了有希望的途径。本综述旨在综合肌肉减少症研究的最新进展,重点关注其发病机制和治疗策略的新贡献。我们探讨了细胞衰老、表观遗传调控和靶向治疗干预等新兴趋势,这些趋势可能重塑未来管理肌肉减少症的方法。通过强调最近的突破和前沿研究,我们希望增进对肌肉减少症的理解,并促进将这些发现转化为有效的临床治疗方法。