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Abstract

ERK = extracellular signal-related kinase; IL = interleukin; JNK = c-Jun N-terminal kinase; MAPK = mitogen-activated protein kinase; MMP = matrix metalloproteinase; RA = rheumatoid arthritis; TNF = tumour necrosis factor. Available online http://arthritis-research.com/content/7/5/177 AbstractMitogen-activated protein kinases (MAPKs) have been associated with the pathogenesis of rheumatoid arthritis (RA), but the individual contributions of the three MAPK family members are incompletely understood. Although previous data have established a role for c-Jun N-terminal kinase (JNK) and extracellular signalrelated kinase (ERK) in different animal models of arthritis, most recent data indicate that the stable activation of p38 MAPK and in part of ERK significantly contributes to destructive arthritis in mice transgenic for human tumour necrosis factor-α. These data highlight the complexity of MAPK signalling in arthritis and provide a basis for the design of novel strategies to treat human RA.

Sigesbeckia orientalis L. Extract Alleviated the Collagen Type II–Induced Arthritis Through Inhibiting Multi-Target–Mediated Synovial Hyperplasia and Inflammation

“…Upstream of NF-κB and AP-1, mitogen-activated protein kinases (MAPKs) are highly active in chronic synovitis and also involved in the regulation of MMP expression ( Schett et al, 2000 ). Three MAPK families including p38, extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK) seem to be involved in the activation of synovial cells in RA ( Meyer and Pap, 2005 ). MAPKs have been implicated in transducing inflammation and joint destruction and therefore are key molecular targets for therapeutic intervention of RA ( Thalhamer et al, 2008 ).…”