TWEAK-Fn14细胞因子-受体轴：发现、生物学特性及治疗靶点
The TWEAK-Fn14 cytokine-receptor axis: discovery, biology and therapeutic targeting.
作者信息
Winkles Jeffrey A
机构信息
Department of Surgery, Center for Vascular and Inflammatory Diseases, and the Marlene and Stewart Greenebaum Cancer Center, 800 West Baltimore Street, University of Maryland School of Medicine, Baltimore, Maryland 21201, USA.
出版信息
Nat Rev Drug Discov. 2008 May;7(5):411-25. doi: 10.1038/nrd2488.
TWEAK is a multifunctional cytokine that controls many cellular activities including proliferation, migration, differentiation, apoptosis, angiogenesis and inflammation. TWEAK acts by binding to Fn14, a highly inducible cell-surface receptor that is linked to several intracellular signalling pathways, including the nuclear factor-kappaB (NF-kappaB) pathway. The TWEAK-Fn14 axis normally regulates various physiological processes, in particular it seems to play an important, beneficial role in tissue repair following acute injury. Furthermore, recent studies have indicated that TWEAK-Fn14 axis signalling may contribute to cancer, chronic autoimmune diseases and acute ischaemic stroke. This Review provides an overview of TWEAK-Fn14 axis biology and summarizes the available data supporting the proposal that both TWEAK and Fn14 should be considered as potential targets for the development of novel therapeutics.
肿瘤坏死因子样弱凋亡诱导因子（TWEAK）是一种多功能细胞因子，可控制多种细胞活动，包括增殖、迁移、分化、凋亡、血管生成和炎症。TWEAK通过与Fn14结合发挥作用，Fn14是一种高度可诱导的细胞表面受体，与多种细胞内信号通路相关，包括核因子-κB（NF-κB）通路。TWEAK-Fn14轴通常调节各种生理过程，特别是在急性损伤后的组织修复中似乎起着重要的有益作用。此外，最近的研究表明，TWEAK-Fn14轴信号传导可能与癌症、慢性自身免疫性疾病和急性缺血性中风有关。本综述概述了TWEAK-Fn14轴生物学，并总结了现有数据，支持将TWEAK和Fn14都视为新型治疗药物开发潜在靶点的提议。
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