Blanco-Colio Luis M, Martín-Ventura Jose L, Munoz-Garcia Begoña, Moreno Juan A, Meilhac Olivier, Ortiz Alberto, Egido Jesus
Vascular Research Lab, Fundacion Jimenez Diaz, Autonoma University, Madrid, Spain.
Front Biosci. 2007 May 1;12:3648-55. doi: 10.2741/2341.
Atherosclerosis is currently described as an inflammatory disease given that the main components of chronic inflammation are present in this process: cell recruitment, proliferation, neovascularization, and sclerosis. Vascular lesions are caused by inflammatory and fibroproliferative responses to injury of the endothelium and vascular smooth muscle cells. Interaction between members of the tumor necrosis factor (TNF) superfamily and their receptors elicits diverse biologic actions that participate in atherosclerosis development. These responses include the expression of adhesion molecules, proinflammatory cytokines, matrix metalloproteinases, and tissue factor, which are known to increase plaque instability. TNF-like weak inducer of apoptosis (TWEAK) is a recently described member of the TNF superfamiliy, which is involved in induction of inflammation, activation of cell growth, and stimulation of apoptosis. In this review, we summarize the potential proatherogenic consequences of the interaction of TWEAK with its receptor Fn14 in the vascular wall.
鉴于慢性炎症的主要成分存在于动脉粥样硬化过程中，包括细胞募集、增殖、新血管形成和硬化，目前动脉粥样硬化被描述为一种炎症性疾病。血管病变是由对内皮细胞和血管平滑肌细胞损伤的炎症和纤维增生反应引起的。肿瘤坏死因子（TNF）超家族成员与其受体之间的相互作用引发了多种参与动脉粥样硬化发展的生物学作用。这些反应包括黏附分子、促炎细胞因子、基质金属蛋白酶和组织因子的表达，已知这些会增加斑块不稳定性。肿瘤坏死因子样凋亡弱诱导剂（TWEAK）是TNF超家族中最近描述的成员，它参与炎症诱导、细胞生长激活和凋亡刺激。在这篇综述中，我们总结了TWEAK与其在血管壁中的受体Fn14相互作用可能产生的促动脉粥样硬化后果。
