The Role of E3 Ligases in Macrophage-mediated Inflammation
E3连接酶在巨噬细胞介导的炎症中的作用作者机构:Zhejiang Key Laboratory of PathophysiologyDepartment of Biochemistry and Molecular BiologyHealth Science CenterNingbo UniversityNingbo 315211China
出 版 物:《生物化学与生物物理进展》 (Progress In Biochemistry and Biophysics)
年 卷 期:2024年第51卷第9期
页 面:2037-2060页
核心收录:
学科分类:0710[理学-生物学] 071010[理学-生物化学与分子生物学] 1002[医学-临床医学] 07[理学] 100214[医学-肿瘤学] 10[医学]
基 金:宁波大学“医学部核心课程建设”项目 国家自然科学基金(32270821) 宁波市自然科学基金(2021J065) 宁波大学王宽诚基金和宁波大学大学生科研创新计划(SRIP)项目(2023SRIP1913)资助
主 题:E3 ligases macrophage NLRs/RLRs/TLRs targeted therapies
摘 要:Macrophages,existed in almost all organs of the body,are responsible for detecting tissue injury,pathogens,playing a key role in host defense against a variety of invading pathogens triggering inflammatory *** evidence suggests that macrophage-mediated immune responses are efficiently regulated by the ubiquitination modification,which is responsible for normal immune ***,numerous studies indicates that the aberrant activation or inhibition of macrophage-mediated immune responses occurs in inflammation,mainly caused by dysregulated ubiquitination modification due to E3 ubiquitin ligases mutations or abnormal ***,E3 ubiquitin ligases,responsible for recognizing the substrates,are key enzymes in the ubiquitin proteasome system(UPS)composed of ubiquitin(Ub),ubiquitin-activating E1 enzymes,ubiquitin-conjugating E2 enzymes,E3 ubiquitin ligases,26S proteasome,and deubiquitinating ***,several E3 ubiquitin ligases are involved in the regulation of some common signal pathways in macrophage-mediated inflammation,including Toll-like receptors(TLRs),nucleotide-binding oligomerization domain(NOD)-like receptors(NLRs),RIG-I-like receptors(RLRs),C-type lectin receptors(CLRs)and the receptor for advanced glycation end products(RAGE).Herein,we summarized the physiological and pathological roles of E3 ligases in macrophage-mediated inflammation,as well as the inhibitors and agonists targeting E3 ligases in macrophage mediated inflammation,providing the new ideas for targeted therapies in macrophage-mediated inflammation caused aberrant function of E3 ligases.