›› 2011, Vol. 31 ›› Issue (12): 1775-.doi: 10.3969/j.issn.1674-8115.2011.12.026

• 综述 • 上一篇    下一篇

趋化因子受体-5相关的心脏移植物血管病变的研究进展

姜兆磊, 何 毅, 梅 举   

  1. 上海交通大学 医学院附属新华医院心胸外科, 上海 200092
  • 出版日期:2011-12-28 发布日期:2012-01-04
  • 通讯作者: 梅 举, 电子信箱: ju_mei@yahoo.cn。
  • 作者简介:姜兆磊(1987—), 男, 硕士生;电子信箱: wojiangzhaolei@163.com。
  • 基金资助:

    上海市科委基金(9411964400);上海市卫生局基金(2008108)

Research progress of chemokine receptor-5 related cardiac allograft vasculopathy

JIANG Zhao-lei, HE Yi, MEI Ju   

  1. Department of Cardiothoracic Surgery, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 200092, China
  • Online:2011-12-28 Published:2012-01-04
  • Supported by:

    Shanghai Science and Technology Committee Foundation, 9411964400;Shanghai Municipal Health Bureau Foundation, 2008108

摘要:

心脏移植物血管病变(CAV)是影响心脏移植物长期存活的主要因素,也是导致受者在术后1年死亡或再次心脏移植的主要原因。目前,普遍认为CAV的发病机制主要是免疫性因素和非免疫性因素共同参与的血管内皮损伤,使血管内膜增厚,最终引起移植心脏缺血。趋化因子及其受体共同参与调控移植物局部的免疫应答。其中,趋化因子受体-5(CCR5)可能在CAV发病机制中起着重要的作用,但其调控CAV的机制目前尚不明确。迄今,CAV的治疗方法仍较为局限;但随着对CCR5研究的不断深入,出现了一些新的研究成果,为CAV的治疗和预防提供了新的方向。

关键词: 心脏移植物血管病变, 趋化因子受体-5, 免疫应答

Abstract:

Cardiac allograft vasculopathy (CAV) continues to limit the long-term success of cardiac transplantation and has become a leading cause for death and retransplantation in patients who survive beyond the first year after heart transplantation. At present, it is considered that both immunologic and nonimmunologic risk factors contribute to the development of CAV by causing endothelial dysfunction and injury, eventually leading to progressive intimal thicking and ischemic failure of the cardiac allograft. Chemokines and their receptors may participate in regulating the local immune response of the graft. Among them, chemokine receptor-5 (CCR5) may play an important role in the pathogenesis of CAV, but the mechanism is unclear. So far, the therapy for CAV has been relatively limited, but there have been some new findings with the research progress of CCR5, which provides a new direction for the treatment and prevention of CAV.

Key words: cardiac allograft vasculopathy, chemokine receptor-5, immune response