Rheumatoid arthritis (RA) is a chronic, autoimmune, and inflammatory disease that primarily targets the joints, leading to cartilage and bone destruction. Fibroblast-like synoviocytes (FLS) are specialized cells of the synovial lining in the joint that plays a fundamental role in the development of RA. Particularly, FLS of RA patients (RA-FLS) in the joint exhibit specific characteristics like higher invading and immunogenic properties, hyperproliferation, and reduced apoptotic capacity, suggesting a dysfunctional mitochondrial pool in these cells. Mitochondria are emerging as a potential organelle that can decide cellular immunometabolism, invasion properties, and cell death. Accordingly, multiple studies established that mitochondria are crucial in establishing RA. However, the underlying mechanism of impaired mitochondrial function in RA remains poorly understood. This review will provide an overview of the mitochondrial role in the progression of RA, specifically in the context of FLS biology. We will also outline how mitochondria-centric therapeutics can be achieved that would yield novel avenues of research in pathological mediation and prevention.

类风湿性关节炎 (RA) 是一种慢性自身免疫性炎症性疾病，主要针对关节，导致软骨和骨质破坏。 成纤维细胞样滑膜细胞 (FLS) 是关节滑膜内层的特殊细胞，在 RA 的发展中发挥着重要作用。特别是，RA患者关节中的FLS（RA-FLS）表现出特定的特征，例如更高的侵袭性和免疫原性、过度增殖和凋亡能力降低，表明这些细胞中线粒体库功能失调。线粒体正在成为一种潜在的细胞器，可以决定细胞免疫代谢、侵袭特性和细胞死亡。因此，多项 研究证实线粒体对于 RA 的形成至关重要。然而，RA 线粒体功能受损的潜在机制仍知之甚少。本综述将概述线粒体在 RA 进展中的作用，特别是在 FLS 生物学背景下。我们还将概述如何实现以线粒体为中心的治疗方法，这将产生病理调节和预防方面的新研究途径。