Metabolite-sensing GPCRs in rheumatoid arthritis

被引：5

作者：

Yang, Xuezhi ^{[1
]}

Zhang, Wankang ^{[1
]}

Wang, Luping ^{[1
]}

Zhao, Yingjie ^{[2
]}

Wei, Wei ^{[1
]}

机构：

[1] Anhui Med Univ, Inst Clin Pharmacol, Key Lab Antiinflammatory & Immune Med, Anhui Collaborat Innovat Ctr Antiinflammatory & Im, Hefei 230032, Peoples R China

[2] Anhui Med Univ, Dept Clin Pharmacol, Affiliated Hosp 2, Hefei 230601, Peoples R China

来源：

TRENDS IN PHARMACOLOGICAL SCIENCES | 2024年 / 45卷 / 02期

基金：

中国国家自然科学基金;

关键词：

GUT-JOINT AXIS; STRUCTURAL BASIS; RECEPTOR; ACTIVATION; DISEASE; GPR35; IDENTIFICATION; SIMILARITIES; CONTRIBUTES; MACROPHAGES;

D O I：

10.1016/j.tips.2023.12.001

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Persistent inflammation in damaged joints results in metabolic dysregulation of the synovial microenvironment, causing pathogenic alteration of cell activity in rheumatoid arthritis (RA). Recently, the role of metabolite and metabolite-sensing G protein-coupled receptors (GPCRs) in the RA-related inflammatory immune response (IIR) has become a focus of research attention. These GPCRs participate in the progression of RA by modulating immune cell activation, migration, and inflammatory responses. Here, we discuss recent evidence implicating metabolic dysregulation in RA pathogenesis, focusing on the connection between RArelated IIR and GPCR signals originating from the synovial joint and gut. Furthermore, we discuss future directions for targeting metabolite-sensing GPCRs for therapeutic benefit, emphasizing the importance of identifying endogenous ligands and investigating the various transduction mechanisms involved.

引用

页码：118 / 133

页数：16

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