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已发表论文
线粒体调节在巨噬细胞极化中的作用：对类风湿关节炎发病机制的意义
Authors Li P , Wang G, Peng Z, Zhang L, Yang F, Wei Y, Pan M, Zang H, Zhou M
Received 19 August 2025
Accepted for publication 16 November 2025
Published 8 December 2025 Volume 2025:18 Pages 17163—17183
DOI https://doi.org/10.2147/JIR.S560635
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Prof. Dr. Yan Chen
Pingshun Li,1,2 Gang Wang,1 Zhihui Peng,3 Lihuan Zhang,1 Fang Yang,1 Yong Wei,1 Meihan Pan,2 Haohao Zang,2 Mengru Zhou1
1Department of Rheumatology and Bone Disease, Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, 730000, People’s Republic of China; 2College of Integrative Chinese and Western Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, People’s Republic of China; 3School of Physical Education and Health, Gansu University of Chinese Medicine, Lanzhou, 730000, People’s Republic of China
Correspondence: Mengru Zhou, Email 931817430@qq.com
Abstract: Rheumatoid arthritis (RA) is an autoimmune arthropathy closely associated with chronic inflammation, whose pathogenesis involves macrophages, particularly M1 macrophage-induced inflammatory responses. Mitochondria, as key organelles governing macrophage metabolism and function, regulate M1/M2 macrophage polarization through multiple pathways and signaling molecules, thereby inducing immune and inflammatory responses that contribute to RA development. Therefore, this paper delves into the intricate mechanisms by which mitochondria regulate macrophage-specific polarization. These pathways encompass metabolic processes, signaling molecules, mitochondrial dynamics, mitochondrial-associated molecules, mitochondrial autophagy, ion homeostasis, and mitochondrial translocation. The study underscores the pivotal role of mitochondria in macrophage-specific polarization and highlights the potential for basic research to intervene in RA by modulating Mitochondrial metabolism, mitochondrial dynamics, mitochondrial autophagy, and mitochondrial translocation to promote M1-to-M2 macrophage conversion and suppress RA inflammatory responses. This holds significant implications for repairing RA-induced bone destruction and advancing clinical treatment.
Keywords: rheumatoid arthritis, macrophages, M1/M2 polarization, inflammatory response, pathogenesis
1Department of Rheumatology and Bone Disease, Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, 730000, People’s Republic of China; 2College of Integrative Chinese and Western Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, People’s Republic of China; 3School of Physical Education and Health, Gansu University of Chinese Medicine, Lanzhou, 730000, People’s Republic of China
Correspondence: Mengru Zhou, Email 931817430@qq.com
Abstract: Rheumatoid arthritis (RA) is an autoimmune arthropathy closely associated with chronic inflammation, whose pathogenesis involves macrophages, particularly M1 macrophage-induced inflammatory responses. Mitochondria, as key organelles governing macrophage metabolism and function, regulate M1/M2 macrophage polarization through multiple pathways and signaling molecules, thereby inducing immune and inflammatory responses that contribute to RA development. Therefore, this paper delves into the intricate mechanisms by which mitochondria regulate macrophage-specific polarization. These pathways encompass metabolic processes, signaling molecules, mitochondrial dynamics, mitochondrial-associated molecules, mitochondrial autophagy, ion homeostasis, and mitochondrial translocation. The study underscores the pivotal role of mitochondria in macrophage-specific polarization and highlights the potential for basic research to intervene in RA by modulating Mitochondrial metabolism, mitochondrial dynamics, mitochondrial autophagy, and mitochondrial translocation to promote M1-to-M2 macrophage conversion and suppress RA inflammatory responses. This holds significant implications for repairing RA-induced bone destruction and advancing clinical treatment.
Keywords: rheumatoid arthritis, macrophages, M1/M2 polarization, inflammatory response, pathogenesis