Guo Zhaojing, Li Hengzhen, Jiang Shide, Rahmati Masoud, Su Jingyue, Yang Shengwu, Wu Yuxiang, Li Yusheng, Deng Zhenhan
Department of Orthopedics, Xiangya Hospital, Central South University, Changsha, China.
Xiangya School of Medicine, Central South University, Changsha, China.
Bone Joint Res. 2025 Mar 4;14(3):185-198. doi: 10.1302/2046-3758.143.BJR-2024-0252.R1.
Sarcopenia is an ageing-related disease featured by the loss of skeletal muscle quality and function. Advanced glycation end-products (AGEs) are a complex set of modified proteins or lipids by non-enzymatic glycosylation and oxidation. The formation of AGEs is irreversible, and they accumulate in tissues with increasing age. Currently, AGEs, as a biomarker of ageing, are viewed as a risk factor for sarcopenia. AGE accumulation could cause harmful effects in the human body such as elevated inflammation levels, enhanced oxidative stress, and targeted glycosylation of proteins inside and outside the cells. Several studies have illustrated the pathogenic role of AGEs in sarcopenia, which includes promoting skeletal muscle atrophy, impairing muscle regeneration, disrupting the normal structure of skeletal muscle extracellular matrix, and contributing to neuromuscular junction lesion and vascular disorders. This article reviews studies focused on the pathogenic role of AGEs in sarcopenia and the potential mechanisms of the detrimental effects, aiming to provide new insights into the pathogenesis of sarcopenia and develop novel methods for the prevention and therapy of sarcopenia.
肌肉减少症是一种与衰老相关的疾病，其特征是骨骼肌质量和功能丧失。晚期糖基化终产物（AGEs）是一组由非酶糖基化和氧化修饰的蛋白质或脂质。AGEs的形成是不可逆的，并且它们会随着年龄的增长在组织中积累。目前，AGEs作为衰老的生物标志物，被视为肌肉减少症的一个危险因素。AGEs的积累会在人体中造成有害影响，如炎症水平升高、氧化应激增强以及细胞内外蛋白质的靶向糖基化。多项研究阐明了AGEs在肌肉减少症中的致病作用，其中包括促进骨骼肌萎缩、损害肌肉再生、破坏骨骼肌细胞外基质的正常结构以及导致神经肌肉接头病变和血管紊乱。本文综述了聚焦于AGEs在肌肉减少症中的致病作用及有害影响潜在机制的研究，旨在为肌肉减少症的发病机制提供新见解，并开发预防和治疗肌肉减少症的新方法。
