New Posttranslational Modification Lactylation Brings New Inspiration for the Treatment of Rheumatoid Arthritis

被引:1
作者
Yang, Yue [1 ]
Shi, Jinjie [2 ]
Yu, Jiming [3 ]
Zhao, Xin [1 ]
Zhu, Ke [1 ]
Wang, Shen [4 ]
Zhang, Xinwen [1 ]
Zhang, Xieyu [1 ]
Wei, Guangcheng [1 ]
Cao, Wei [1 ]
机构
[1] China Acad Chinese Med Sci, Wangjing Hosp, Rheumatol Dept, Beijing, Peoples R China
[2] Beijing Univ Chinese Med, Grad Sch, Beijing, Peoples R China
[3] Henan Univ Chinese Med, Clin Med Coll 2, Zhengzhou, Peoples R China
[4] Nanjing Integrated Tradit Chinese & Western Med Ho, Orthoped Dept, Nanjing, Peoples R China
基金
中国国家自然科学基金;
关键词
lactic acid; lactylation; posttranslational modification; rheumatoid arthritis; PROTEASOME INHIBITION; INFLAMMATORY-DISEASES; HISTONE LACTYLATION; SYNOVIAL-FLUID; LACTATE; METABOLISM; MACROPHAGES; PATHWAY; PROTEIN; CELLS;
D O I
10.2147/JIR.S497240
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Lactic acid (LA) is an essential glycolytic metabolite and energy source in the body, which is present in high levels in the synovial fluid of patients with rheumatoid arthritis (RA) and is a reliable indicator for identifying inflammatory arthritis. LA not only acts as an inflammatory amplifier in RA, recent studies have found that novel posttranslational modification (PTM) lactylation mediated by LA may also play a key role in RA. Single-cell sequencing showed that the RA lactylation score of patients with RA was significantly increased, and core lactylation-promoting genes, including NDUFB3, NGLY1, and other genes, were found to be potential biomarkers of RA. More studies have shown that lactylation can regulate genes in various cells, such as fibroblast-like synoviocytes (FLSs) and macrophages, thus playing a special role in the development and occurrence of autoimmune diseases, neurological diseases, and cancer diseases. In this paper, we review the research on lactylation in RA-related cells and mechanisms and bring new insights into the pathogenesis, diagnosis, and treatment of RA.
引用
收藏
页码:11845 / 11860
页数:16
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