tailieunhanh - Báo cáo y học: "Tyrosine kinases in rheumatoid arthritis"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Tyrosine kinases in rheumatoid arthritis. | Okamoto and Kobayashi Journal of Inflammation 2011 8 21 http content 8 1 21 REVIEW JOURNAL OF INFLAMMATION Open Access Tyrosine kinases in rheumatoid arthritis Hiroshi Okamoto and Akiko Kobayashi Abstract Rheumatoid arthritis RA is an inflammatory polyarticular joint disease. A number of cellular responses are involved in the pathogenesis of rheumatoid arthritis including activation of inflammatory cells and cytokine expression. The cellular responses involved in each of these processes depends on the specific signaling pathways that are activated many of which include protein tyrosine kinases. These pathways include the mitogen-activated protein kinase pathway Janus kinases signal transducers and activators transcription pathway spleen tyrosine kinase signaling and the nuclear factor K-light-chain-enhancer of activated B cells pathway. Many drugs are in development to target tyrosine kinases for the treatment of RA. Based on the number of recently published studies this manuscript reviews the role of tyrosine kinases in the pathogenesis of RA and the potential role of kinase inhibitors as new therapeutic strategies of RA. Introduction Rheumatoid arthritis RA is a destructive inflammatory polyarticular joint disease with an etiology that remains to be fully elucidated. RA is characterized by massive synovial proliferation and subintimal infiltration of inflammatory cells followed by the destruction of cartilage and bone 1 . A number of cellular responses are involved in the pathogenesis of RA including activation of inflammatory cells and expression of various cytokines. Macrophages T cells B cells and neutrophils migrate into synovial tissue and activate these cells to produce both inflammatory and degradative mediators that break down the extracellular matrix of cartilage. Synovial cells undergo hyperplasia and angiogenesis occurs in synovial tissues further promoting inflammation. Although synoviocyte proliferation contributes to the