E3泛素连接酶在肌少症中的作用机制研究进展  

Recent Advances in the Mechanism of Action of E3 Ubiquitin Ligases in Sarcopenia

作　　者：史雪珂 代婷 王亚敏 高静 刘楠楠 冯晓东[2] SHI Xue-Ke;DAI Ting;WANG Ya-Min;GAO Jing;LIU Nan-Nan;FENG Xiao-Dong(Rehabilitation Medicine College,Henan University of Chinese Medicine,Zhengzhou 450046,China;The First Affiliated Hospital of Henan University of Chinese Medicine,Zhengzhou 450000,China)

机构地区：[1]河南中医药大学康复医学院,郑州450046 [2]河南中医药大学第一附属医院,郑州450000

出　　处：《生理科学进展》2025年第1期90-96,共7页Progress in Physiological Sciences

基　　金：国家重点研发计划中医药现代化研究专项(2023YFC3503705)资助课题。

摘　　要：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.

关 键 词：E3泛素连接酶 肌少症 肌肉萎缩盒F蛋白 肌肉特异性环指蛋白1 

分 类 号：R685[医药卫生—骨科学]