Abstract

RA is an incurable systemic inflammation the main features are infiltration of pro-inflammatory factors with joint swelling and pain as the main clinical manifestation. Studies have shown that there are many causes of RA, among which immune factors are the most important pathogenesis of rheumatoid arthritis. At present, emerging studies have found that PI3K / AKT / mTOR signaling axis is abnormal in patients with RA, which opens up new ideas for the treatment of RA through the normal expression of signal transduction by targeted drugs. Janus kinase family ( JAKs ), are up-regulated in non-receptor protein tyrosine kinase cytokine signaling ( SOCS ) inhibitors, suggesting that the existence of SOCS is most possibly to constitute the main machine-made of negative adjustment of JAK / STAT signaling. In RA patients, there is a correlation between the activation of mTOR signaling and the quantity of osteoclasts. The recently discovered cytokine IL-22 has been shown to significantly increase the number of fibroblasts isolated from the skin of the patients with psoriasis. The dual inhibitor of P1-3K / mTOR, NVP-BEZ235, effectively blocks the spread. This article mainly explores and discusses new targeted drugs such as tofacitinib and Ruxolitinib by discussing new pathological mechanisms and conventional diagnosis and treatment methods of RA. Since RA is one of the most representative diseases of skeletal immune diseases, the study of ra abnormal signaling pathways to discuss related treatment methods provides valuable insights into the disease and other inflammatory and autoimmune diseases.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call