Camandola Simonetta, Mattson Mark P
Laboratory of Neurosciences, National Institute onAging, Intramural Research Program, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA.
Expert Opin Ther Targets. 2007 Feb;11(2):123-32. doi: 10.1517/14728222.11.2.123.
NF-kappaB is a transcription factor that regulates numerous physiological functions, and that is involved in the pathogenesis of various diseases. In the nervous system there is evidence supporting a dual role of NF-kappaB in neurodegenerative diseases; activation of NF-kappaB in neurons promotes their survival, whereas activation in glial and immune cells mediates pathological inflammatory processes. The reason for such a dichotomy lies in the complexity of the NF-kappaB system. Emerging research has begun to dissect the pathways leading to the activation of the different NF-kappaB proteins, and the gene targets of NF-kappaB, in cells of the nervous system. In this article the authors discuss recent findings concerning the roles of NF-kappaB in the pathogenesis of several neurodegenerative disorders, and its potential as a pharmaceutical target for these disorders.
核因子-κB是一种调节多种生理功能的转录因子,并且参与多种疾病的发病机制。在神经系统中,有证据支持核因子-κB在神经退行性疾病中具有双重作用;神经元中核因子-κB的激活促进其存活,而胶质细胞和免疫细胞中的激活介导病理性炎症过程。这种二分法的原因在于核因子-κB系统的复杂性。新兴研究已开始剖析导致神经系统细胞中不同核因子-κB蛋白激活的途径以及核因子-κB的基因靶点。在本文中,作者讨论了关于核因子-κB在几种神经退行性疾病发病机制中的作用及其作为这些疾病药物靶点的潜力的最新研究发现。