Role of reactive oxygen species and mitochondrial damage in rheumatoid arthritis and targeted drugs

Weiyao Jing; Cui Liu; Chenghong Su; Limei Liu; Ping Chen; Xiangjun Li; Xinghua Zhang; Bo Yuan; Haidong Wang; Xiaozheng Du

doi:10.3389/fimmu.2023.1107670

Role of reactive oxygen species and mitochondrial damage in rheumatoid arthritis and targeted drugs

Front Immunol. 2023 Feb 9:14:1107670. doi: 10.3389/fimmu.2023.1107670. eCollection 2023.

Authors

Weiyao Jing¹, Cui Liu¹, Chenghong Su¹, Limei Liu¹, Ping Chen², Xiangjun Li², Xinghua Zhang³, Bo Yuan⁴, Haidong Wang², Xiaozheng Du¹

Affiliations

¹ Department of Acupuncture-Moxibustion and Tuina, Gansu University of Chinese Medicine, Lanzhou, China.
² Department of Rheumatic and Bone Disease, Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou, China.
³ Department of Acupuncture, Gansu Provincial Hospital of Traditional Chinese Medicine, Lanzhou, China.
⁴ Department of Acupuncture and Pain, Affiliated Hospital of Gansu University of Traditional Chinese Medicine, Lanzhou, China.

Abstract

Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial inflammation, pannus formation, and bone and cartilage damage. It has a high disability rate. The hypoxic microenvironment of RA joints can cause reactive oxygen species (ROS) accumulation and mitochondrial damage, which not only affect the metabolic processes of immune cells and pathological changes in fibroblastic synovial cells but also upregulate the expression of several inflammatory pathways, ultimately promoting inflammation. Additionally, ROS and mitochondrial damage are involved in angiogenesis and bone destruction, thereby accelerating RA progression. In this review, we highlighted the effects of ROS accumulation and mitochondrial damage on inflammatory response, angiogenesis, bone and cartilage damage in RA. Additionally, we summarized therapies that target ROS or mitochondria to relieve RA symptoms and discuss the gaps in research and existing controversies, hoping to provide new ideas for research in this area and insights for targeted drug development in RA.

Keywords: mitochondrial damage; oxidative stress; reactive oxygen species; rheumatoid arthritis; targeted drugs.

Publication types

Review
Research Support, Non-U.S. Gov't

MeSH terms

Arthritis, Rheumatoid*
Bone and Bones / metabolism
Humans
Inflammation / metabolism
Reactive Oxygen Species / metabolism
Synovial Membrane*

Substances

Reactive Oxygen Species

Grants and funding

The National Natural Science Foundation of China (No. 82060891), Natural Science Foundation of Gansu Province (No. 21JR7RA568, No. 22JR5RA637), 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.