类风湿性关节炎
促炎细胞因子
贾纳斯激酶
医学
发病机制
细胞因子
蛋白激酶A
脱颗粒
关节炎
激酶
炎症
p38丝裂原活化蛋白激酶
癌症研究
信号转导
免疫学
内科学
生物
细胞生物学
受体
作者
Rakesh Kumar Chauhan,Pramod Kumar Sharma,Shikha Srivastava
出处
期刊:Current drug research reviews
[Bentham Science]
日期:2020-11-11
卷期号:13 (2): 130-139
被引量:3
标识
DOI:10.2174/2589977512999201109215004
摘要
Rheumatoid arthritis not only affects synovial joints but also many other sites including heart, blood vessels, and skins. It is more common in females than in males. The exact cause of rheumatoid arthritis is not well established, but the hypothesis reported in the literature is that in the development stage of the disease, both genetics and environmental factors can play an inciting role. Along with these factors, the alteration in the normal physiology of enzymatic action acts as a trigger to develop this condition. Numerous signaling pathways in the pathogenesis of Rheumatoid Arthritis involve activation of mitogen-activated protein kinase, kinases Janus family, P-38 Mitogen- Activated Protein Kinase and Nuclear Factor-kappa B. Interleukin-1, is a proinflammatory cytokine that plays an important role in inflammation in RA. These are also associated with an increase in neutrophil, macrophage and lymphocytic chemotaxis, mast cell degranulation, activation, maturation and survival of T-cells and B-cells activated. These signaling pathways also show that p38α downregulation in myeloid cells exacerbates the severity of symptoms of arthritis. Thus, the present review carters about the detail of different signaling pathways and their role in rheumatoid arthritis.
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