文献类型：期刊文献

英文题名：The Role of Mitochondrial Regulation in Macrophage Polarization: Implications for the Pathogenesis of Rheumatoid Arthritis

作者：Li, Pingshun[1,2];Wang, Gang[1];Peng, Zhihui[3];Zhang, Lihuan[1];Yang, Fang[1];Wei, Yong[1];Pan, Meihan[2];Zang, Haohao[2];Zhou, Mengru[1]

第一作者：Li, Pingshun

通信作者：Zhou, MR[1]

机构：[1]Gansu Univ Chinese Med, Affiliated Hosp, Dept Rheumatol & Bone Dis, Lanzhou 730000, Peoples R China;[2]Gansu Univ Chinese Med, Coll Integrat Chinese & Western Med, Lanzhou 730000, Peoples R China;[3]Gansu Univ Chinese Med, Sch Phys Educ & Hlth, Lanzhou 730000, Peoples R China

第一机构：甘肃中医药大学第二附属医院

通信机构：[1]corresponding author), Gansu Univ Chinese Med, Affiliated Hosp, Dept Rheumatol & Bone Dis, Lanzhou 730000, Peoples R China.|[10735b845793de6ae2b30]甘肃中医药大学第二附属医院;[10735]甘肃中医药大学;

年份：2025

卷号：18

起止页码：17163

外文期刊名：JOURNAL OF INFLAMMATION RESEARCH

收录：;Scopus(收录号：2-s2.0-105024188772);WOS:【SCI-EXPANDED(收录号:WOS:001666661700001)】；

基金：Supported by the Gansu Provincial Natural Science Foundation Youth Fund Program (No.22JR11RA133, 21JR11RA158) , The Second Affiliated Hospital of Gansu University of Traditional Chinese Medicine Youth Program (No. ZX-62000004-2022-092) , Gansu Province Famous Traditional Chinese Medicine Practitioners Inheritance Studio Construction Project (National TCM Regulation and Caixin Letter [2021] No. 50) and 2023 Central Finance Transfer Payment for Local Projects for Capacity Enhancement of Chinese Medicine Counseling and Evidence Construction (No. 2101704) .

语种：英文

外文关键词：rheumatoid arthritis; macrophages; M1/M2 polarization; inflammatory response; pathogenesis

摘要：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 ostasis, 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.