Department of Physiology and Pathophysiology, School of Basic Medicine, Shandong University, Jinan, China.
Department of Emergency, Qilu Hospital of Shandong University, Jinan, China.
Am J Pathol. 2018 Apr;188(4):838-845. doi: 10.1016/j.ajpath.2017.12.002. Epub 2018 Jan 16.
Transplant vasculopathy is one of the major causes of chronic rejection after solid organ transplantation. The pathogenic mechanisms of transplant vasculopathy are still poorly understood. Herein, we summarize current evidence suggesting that activation of the tunica adventitia may be involved in the pathogenesis of transplant vasculopathy. Adventitia is an early responder to various vascular injuries and plays an integral role in eliciting vascular inflammation and remodeling. Accumulation of macrophages in the adventitia promotes the development of vascular remodeling by releasing a variety of paracrine factors that have profound impacts on vascular mural cells. Targeting adventitial macrophages has been shown to be effective for repressing transplantation-induced arterial remodeling in animal models. Adventitia also fosters angiogenesis, and neovascularization of the adventitial layer may facilitate the transport of inflammatory cells through the arterial wall. Further investigations are warranted to clarify whether inhibiting adventitial oxidative stress and/or adventitial neovascularization are better strategies for preventing transplant vasculopathy.
移植血管病是实体器官移植后慢性排斥反应的主要原因之一。移植血管病的发病机制仍不清楚。在此，我们总结了目前的证据，表明中膜鞘的激活可能参与了移植血管病的发病机制。中膜鞘是对各种血管损伤的早期反应者，在引发血管炎症和重塑中起着重要作用。中膜鞘内巨噬细胞的积累通过释放各种旁分泌因子促进血管重塑，这些因子对血管壁细胞有深远影响。靶向中膜鞘巨噬细胞已被证明可有效抑制动物模型中移植诱导的动脉重塑。中膜鞘还促进血管生成，中膜鞘的新生血管化可能有助于炎症细胞通过动脉壁的运输。进一步的研究是必要的，以明确抑制中膜鞘氧化应激和/或中膜鞘新生血管化是否是预防移植血管病的更好策略。
