摘要
系统性红斑狼疮(systemic lupus erythematosus,SLE)是抗核抗体大量产生、多器官炎症的自身免疫性疾病,严重损害患者的生活质量,给医疗保健系统带来沉重负担.尽管SLE的发病机制目前尚不完全明确,但近年来,表观遗传调控和翻译后修饰在该疾病中的作用逐渐受到科学家的关注.其中,泛素化作为一种重要的蛋白质修饰方式,在维持蛋白质稳态和蛋白质间相互作用的平衡中发挥着关键作用.去泛素化酶通过调控关键靶点蛋白质的稳态,对SLE的发病机制和进程产生了深远的影响.本综述回顾SLE与蛋白质去泛素化的已有研究,旨在为SLE新治疗靶点的开发提供新思路.
Systemic lupus erythematosus(SLE)is an autoimmune disease characterized by the production of anti-nuclear antibodies and widespread organ inflammation.The pathogenesis of SLE is not yet fully understood,however,recent research have increasingly focused on the role of epigenetic regulation and post-translational modifications in this disease.Among these,ubiquitination,as an important form of protein modification,plays a key role in maintaining protein homeostasis and the balance of protein-protein interactions.Deubiquitinating enzymes(DUBs),by regulating the homeostasis of key target proteins,have exerted profound effects on the pathogenic mechanisms and progression of SLE.This review aims to provide insights into the existing research on SLE and deubiquitination,focusing on molecular mechanisms,with the goal of providing new perspectives for the development of novel therapeutic targets for SLE.
作者
赵明久
谷梦瑶
骆文君
张梦迪
黄佳琦
赵斌
ZHAO MingJiu;GU MengYao;LUO WenJun;ZHANG MengDi;HUANG JiaQi;ZHAO Bin(National Clinical Research Center for Metabolic Diseases,Metabolic Syndrome Research Center,Key Laboratory of Diabetes Immunology,Ministry of Education,and Department of Metabolism and Endocrinology,The Second Xiangya Hospital of Central South University,Changsha 410011,China;Furong Laboratory,Changsha 410013,China;CSU-Sinocare Research Center for Nutrition and Metabolic Health,Xiangya School of Public Health,Central South University,Changsha 410013,China)
出处
《中国科学:生命科学》
CSCD
北大核心
2024年第11期2143-2153,共11页
Scientia Sinica(Vitae)
基金
国家自然科学基金(资助号:81820108007、82170795和82100949)
湖南省自然科学基金(资助号:2021JC0003和2023JJ30805)
湖南省杰出青年科学基金(资助号:2022JJ10094)
中南大学高级交叉研究计划(资助号:2023QYJC008)资助。
关键词
去泛素化
系统性红斑狼疮
免疫细胞
自身免疫疾病
deubiquitination
systemic lupus erythematosus
immune cells
autoimmune disease