Li Pingshun, Zhou Mengru, Wang Jia, Tian Jiexiang, Zhang Lihuan, Wei Yong, Yang Fang, Xu Yali, Wang Gang
College of Integrative Chinese and Western Medicine, Gansu University of Chinese Medicine, Lanzhou, 730000, People's Republic of China.
Department of Rheumatology and Bone Disease, Affiliated Hospital of Gansu University of Chinese Medicine, Lanzhou, 730000, People's Republic of China.
J Inflamm Res. 2024 Dec 27;17:11631-11657. doi: 10.2147/JIR.S499473. eCollection 2024.
Rheumatoid arthritis (RA) is an inflammatory autoimmune disease, primarily characterized by chronic symmetric synovial inflammation and erosive bone destruction.Mitochondria, the primary site of cellular energy production, play a crucial role in energy metabolism and possess homeostatic regulation capabilities. Mitochondrial function influences the differentiation, activation, and survival of both immune and non-immune cells involved in RA pathogenesis. If the organism experiences hypoxia, genetic predisposition, and oxidative stress, it leads to mitochondrial dysfunction, which further affects immune cell energy metabolism, synovial cell proliferation, apoptosis, and inflammatory signaling, causing the onset and progression of RA; and, mitochondrial regulation is becoming increasingly important in the treatment of RA.In this review, we examine the structure and function of mitochondria, analyze the potential causes of mitochondrial dysfunction in RA, and focus on the mechanisms by which mitochondrial dysfunction triggers chronic inflammation and immune disorders in RA. We also explore the effects of mitochondrial dysfunction on RA immune cells and osteoblasts, emphasizing its key role in the immune response and inflammatory processes in RA. Furthermore, we discuss potential biological processes that regulate mitochondrial homeostasis, which are of great importance for the prevention and treatment of RA.
类风湿关节炎（RA）是一种炎症性自身免疫疾病，主要特征为慢性对称性滑膜炎和侵蚀性骨破坏。线粒体作为细胞能量产生的主要场所，在能量代谢中发挥关键作用，并具备稳态调节能力。线粒体功能影响参与RA发病机制的免疫细胞和非免疫细胞的分化、激活及存活。若机体遭遇缺氧、遗传易感性和氧化应激，会导致线粒体功能障碍，进而影响免疫细胞能量代谢、滑膜细胞增殖、凋亡及炎症信号传导，引发RA的发病与进展；并且，线粒体调节在RA治疗中愈发重要。在本综述中，我们研究线粒体的结构与功能，分析RA中线粒体功能障碍的潜在成因，并聚焦线粒体功能障碍引发RA慢性炎症和免疫紊乱的机制。我们还探讨线粒体功能障碍对RA免疫细胞和成骨细胞的影响，强调其在RA免疫反应和炎症过程中的关键作用。此外，我们讨论调节线粒体稳态的潜在生物学过程，这对RA的预防和治疗至关重要。
