Müller-Ladner Ulf, Gay Renate E, Gay Steffen
Department of Internal Medicine I, University of Regensburg, D-93042 Regensburg, Germany.
Curr Rheumatol Rep. 2002 Jun;4(3):201-7. doi: 10.1007/s11926-002-0066-1.
The evaluation of molecular pathways has revealed novel insights into the pathophysiology of rheumatoid arthritis in the last several years. Gene transcription factors such as nuclear factor kB (NFkB) are activated by extracellular signals or cell-to-cell interactions that are converted into intracellular activation signals through receptor molecules located in the cell membrane. The number of known genes being translated after NFkB activation is increasing steadily. These genes includes cytokines, chemokines, growth factors, cellular ligands, and adhesion molecules. Because many of these genes are part of the pathogenesis of RA, there is considerable interest in the evaluation of the synovium-specific effects of NFkB to unveil its potential for future therapeutic strategies. The goal is to evolve these strategies from the therapies that have a wide spectrum of effects and side effects into rheumatoid arthritis-specific therapies designed to inhibit distinct molecular pathways within the synovium.
在过去几年中，对分子途径的评估为类风湿性关节炎的病理生理学带来了新的见解。诸如核因子κB（NFκB）等基因转录因子可被细胞外信号或细胞间相互作用激活，这些信号通过位于细胞膜上的受体分子转化为细胞内激活信号。NFκB激活后被翻译的已知基因数量正在稳步增加。这些基因包括细胞因子、趋化因子、生长因子、细胞配体和黏附分子。由于这些基因中的许多都是类风湿性关节炎发病机制的一部分，因此人们对评估NFκB的滑膜特异性效应以揭示其在未来治疗策略中的潜力有着浓厚的兴趣。目标是将这些策略从具有广泛效应和副作用的疗法发展为旨在抑制滑膜内不同分子途径的类风湿性关节炎特异性疗法。
