MAPK signalling in rheumatoid joint destruction: can we unravel the puzzle?
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* Corresponding author: Thomas Pap thomas.pap@uni-muenster.de
Division of Molecular Medicine of Musculoskeletal Tissue, Department of Orthopaedics, University Hospital of Munster, Munster, Germany
Arthritis Research & Therapy 2005, 7:177-178 doi:10.1186/ar1810
Published: 16 August 2005Abstract
Mitogen-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 signal-related 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.