Meyer Lars-Henrik, Pap Thomas
Division of Molecular Medicine of Musculoskeletal Tissue, Department of Orthopaedics, University Hospital of Munster, Munster, Germany.
Arthritis Res Ther. 2005;7(5):177-8. doi: 10.1186/ar1810. Epub 2005 Aug 16.
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-alpha. These data highlight the complexity of MAPK signalling in arthritis and provide a basis for the design of novel strategies to treat human RA.
丝裂原活化蛋白激酶（MAPKs）与类风湿性关节炎（RA）的发病机制有关，但对MAPK家族三个成员各自的作用了解并不完全。虽然先前的数据已证实c-Jun氨基末端激酶（JNK）和细胞外信号调节激酶（ERK）在不同的关节炎动物模型中发挥作用，但最新数据表明，p38 MAPK的稳定激活以及部分ERK的激活，在人肿瘤坏死因子-α转基因小鼠的破坏性关节炎中起重要作用。这些数据突显了关节炎中MAPK信号传导的复杂性，并为设计治疗人类RA的新策略提供了依据。
