Jung In-Hyuk, Oh Goo Taeg
Department of Life Sciences, Ewha Womans University, Seoul, Korea.; Cardiovascular Division, Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA.
Department of Life Sciences, Ewha Womans University, Seoul, Korea.
Korean Circ J. 2016 Nov;46(6):753-761. doi: 10.4070/kcj.2016.46.6.753. Epub 2016 Oct 20.
The tumor necrosis factor receptor superfamily (TNFRSF), which includes CD40, LIGHT, and OX40, plays important roles in the initiation and progression of cardiovascular diseases, involving atherosclerosis. CD137, a member of TNFRSF, is a well-known activation-induced T cell co-stimulatory molecule and has been reported to be expressed in human atherosclerotic plaque lesions, and plays pivotal roles in mediating disease processes. In this review, we focus on and summarize recent advances in mouse studies on the involvement of CD137 signaling in the pathogenesis and plaque stability of atherosclerosis, thereby highlighting a valuable therapeutic target in atherosclerosis.
肿瘤坏死因子受体超家族(TNFRSF),包括CD40、LIGHT和OX40,在心血管疾病(包括动脉粥样硬化)的发生和发展中起重要作用。CD137是TNFRSF的成员之一,是一种著名的激活诱导型T细胞共刺激分子,据报道在人类动脉粥样硬化斑块病变中表达,并在介导疾病过程中起关键作用。在本综述中,我们重点关注并总结了小鼠研究中关于CD137信号通路参与动脉粥样硬化发病机制和斑块稳定性的最新进展,从而突出了动脉粥样硬化中一个有价值的治疗靶点。