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.%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.
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