摘要
TWEAK是肿瘤坏死因子(TNF)家族的新成员,TWEAK与其受体Fn14结合后可引起广泛的生物学活性。TWEAK-Fn14通路在中枢神经系统中参与了细胞凋亡、血脑屏障通透性的调节、炎症反应等病理生理学机制,并与缺血性卒中、多发性硬化以及胶质细胞瘤等疾病密切相关。
Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) is a new member of the tumor necrosis factor farnily. After TWEAK binding to its receptor Fnl4, it induces extensixe biological activities. TWEAK-Fnl4 ~y participates in pathophysiological mechanisms of cell apoptosis, regulation of the blood-brain barrier permeability and inflammation in central ner^us system, and it is closely correlated with the diseases such as ischernic stroke, multiple sclerosis and gliocytoma.
出处
《国际脑血管病杂志》
2008年第5期384-387,共4页
International Journal of Cerebrovascular Diseases