肌少症(sarcopenia)是一种与年龄相关的全身性骨骼肌疾病,严重影响老年人的健康和生活质量,是导致老年人残疾和社会负担加重的主要原因之一。蛋白质合成与降解失衡是其主要发病机制,其中以E3泛素连接酶(ubiquitin ligases)为核心的泛素蛋白酶体系统(ubiquitin proteasome system)在调节肌肉蛋白质降解中起着关键作用。本文阐述并总结了E3泛素连接酶在肌少症相关肌肉萎缩中的作用与机制,旨在为肌少症的基础研究、治疗靶点的发现及相关预防策略的制定提供新思路。

Sarcopenia is an age-related, systemic skeletal muscle disease that severely affects the health and quality of life of the elderly, serving as one of the leading causes of disability and increased social burden among this population. The imbalance between protein synthesis and degradation is a primary pathogenic mechanism, in which the ubiquitin-proteasome system (UPS), particularly E3 ubiquitin ligases (E3s), plays a crucial role in regulating muscle protein degradation. This article elucidates and summarizes the impact and mechanisms of E3s in sarcopenia-associated muscle atrophy, aiming to provide novel insights for basic research, the identification of therapeutic targets, and the development of preventive strategies for sarcopenia.