Department of Pharmacology, SVKM's Dr. Bhanuben Nanavati College of Pharmacy, V.M. Road, Vile Parle (W), Mumbai, India.
Endocr Metab Immune Disord Drug Targets. 2024;24(3):291-301. doi: 10.2174/0118715303250834230923234802.
Rheumatoid arthritis (RA) is characterized by synovial edema, inflammation, bone and cartilage loss, and joint degradation. Patients experience swelling, stiffness, pain, limited joint movement, and decreased mobility as the condition worsens. RA treatment regimens often come with various side effects, including an increased risk of developing cancer and organ failure, potentially leading to mortality. However, researchers have proposed mechanistic hypotheses to explain the underlying causes of synovitis and joint damage in RA patients. This review article focuses on the role of synoviocytes and synoviocytes resembling fibroblasts in the RA synovium. Additionally, it explores the involvement of epigenetic regulatory systems, such as microRNA pathways, silent information regulator 1 (SIRT1), Peroxisome proliferatoractivated receptor-gamma coactivator (PGC1-α), and protein phosphatase 1A (PPM1A)/high mobility group box 1 (HMGB1) regulators. These mechanisms are believed to modulate the function of receptors, cytokines, and growth factors associated with RA. The review article includes data from preclinical and clinical trials that provide insights into potential treatment options for RA.
类风湿关节炎（RA）的特征是滑膜水肿、炎症、骨和软骨损失以及关节退化。随着病情的恶化，患者会出现肿胀、僵硬、疼痛、关节运动受限和活动能力下降等症状。RA 的治疗方案通常伴随着各种副作用，包括癌症和器官衰竭风险增加，可能导致死亡。然而，研究人员提出了机制假说，以解释 RA 患者滑膜炎症和关节损伤的根本原因。这篇综述文章重点介绍了滑膜细胞和成纤维细胞样滑膜细胞在 RA 滑膜中的作用。此外，还探讨了表观遗传调节系统的参与，如 microRNA 途径、沉默信息调节因子 1（SIRT1）、过氧化物酶体增殖物激活受体-γ共激活因子（PGC1-α）和蛋白磷酸酶 1A（PPM1A）/高迁移率族蛋白 1（HMGB1）调节剂。这些机制被认为可以调节与 RA 相关的受体、细胞因子和生长因子的功能。综述文章包括来自临床前和临床试验的数据，这些数据为 RA 的潜在治疗选择提供了新的思路。
