关键词: Rheumatoid arthritis fibroblast high mobility group box 1 inflammation. peroxisome proliferator-activated receptor coactivator-1 protein phosphatase 1A silent information regulator 1 synoviocytes

Mesh : Humans Arthritis, Rheumatoid / metabolism drug therapy Animals Antirheumatic Agents / therapeutic use Synoviocytes / metabolism drug effects pathology Epigenesis, Genetic / physiology drug effects Synovial Membrane / metabolism pathology drug effects Signal Transduction / drug effects

来  源:   DOI:10.2174/0118715303250834230923234802

Abstract:
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.
摘要:
类风湿性关节炎(RA)的特征是滑膜水肿,炎症,骨和软骨损失,联合退化。患者经历肿胀,刚度,疼痛,有限的关节运动,随着病情恶化,流动性下降。RA治疗方案往往伴随着各种副作用,包括患癌症和器官衰竭的风险增加,有可能导致死亡。然而,研究人员提出了机械性的假设来解释RA患者滑膜炎和关节损伤的根本原因.本文重点介绍滑膜细胞和类似成纤维细胞的滑膜细胞在RA滑膜中的作用。此外,它探讨了表观遗传调控系统的参与,如microRNA通路,静默信息调节器1(SIRT1),过氧化物酶体增殖物激活受体-γ共激活剂(PGC1-α),和蛋白磷酸酶1A(PPM1A)/高迁移率族蛋白1(HMGB1)调节因子。这些机制被认为是调节受体的功能,细胞因子,和与RA相关的生长因子。这篇综述文章包括来自临床前和临床试验的数据,这些数据提供了对RA潜在治疗方案的见解。
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