文献类型：期刊文献

英文题名：Rheumatoid arthritis and mitochondrial homeostasis: The crossroads of metabolism and immunity

作者：Cui, Liu[1];Weiyao, Jing[1];Chenghong, Su[1];Limei, Liu[1];Xinghua, Zhang[2];Bo, Yuan[3];Xiaozheng, Du[1];Haidong, Wang[4]

第一作者：Cui, Liu

通信作者：Xiaozheng, D[1];Haidong, W[2]

机构：[1]Gansu Univ Chinese Med, Coll Acupuncture Moxibust & Tuina, Lanzhou, Peoples R China;[2]Gansu Prov Hosp Tradit Chinese Med TCM, Acupuncture & Moxibust Dept, Lanzhou, Peoples R China;[3]Gansu Univ Tradit Chinese Med TCM, Acupuncture & Pain Dept, Affiliated Hosp, Lanzhou, Peoples R China;[4]Gansu Prov Hosp Tradit Chinese Med TCM, Rheumatoid Bone Dis Ctr, Lanzhou, Peoples R China

第一机构：甘肃中医药大学针灸推拿学院

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Coll Acupuncture Moxibust & Tuina, Lanzhou, Peoples R China;[2]corresponding author), Gansu Prov Hosp Tradit Chinese Med TCM, Rheumatoid Bone Dis Ctr, Lanzhou, Peoples R China.|[10735db5df93766a96e5b]甘肃中医药大学针灸推拿学院;[10735]甘肃中医药大学;

年份：2022

卷号：9

外文期刊名：FRONTIERS IN MEDICINE

收录：;Scopus(收录号：2-s2.0-85140057706);WOS:【SCI-EXPANDED(收录号:WOS:000869026800001)】；

基金：This work was supported by the National Natural Science Foundation of China (No. 82060891), Natural Science Foundation of Gansu Province (No. 21JR7RA568), Project of Zheng's Acupuncture Academic Schools of Heritage Studio, Gansu Province, State Administration of TCM (No. 2305135901), and Gansu Province Youth Science and Technology Fund (No. 20JR10RA344) funded the study.

语种：英文

外文关键词：rheumatoid arthritis; mitochondrial homeostasis; energy metabolism; immune cells; apoptosis and proliferation; inflammatory pathways

摘要：Rheumatoid arthritis is an autoimmune disease characterized by chronic symmetric synovial inflammation and erosive bone destruction. Mitochondria are the main site of cellular energy supply and play a key role in the process of energy metabolism. They possess certain self-regulatory and repair capabilities. Mitochondria maintain relative stability in number, morphology, and spatial structure through biological processes, such as biogenesis, fission, fusion, and autophagy, which are collectively called mitochondrial homeostasis. An imbalance in the mitochondrial homeostatic environment will affect immune cell energy metabolism, synovial cell proliferation, apoptosis, and inflammatory signaling. These biological processes are involved in the onset and development of rheumatoid arthritis. In this review, we found that in rheumatoid arthritis, abnormal mitochondrial homeostasis can mediate various immune cell metabolic disorders, and the reprogramming of immune cell metabolism is closely related to their inflammatory activation. In turn, mitochondrial damage and homeostatic imbalance can lead to mtDNA leakage and increased mtROS production. mtDNA and mtROS are active substances mediating multiple inflammatory pathways. Several rheumatoid arthritis therapeutic agents regulate mitochondrial homeostasis and repair mitochondrial damage. Therefore, modulation of mitochondrial homeostasis would be one of the most attractive targets for the treatment of rheumatoid arthritis.