Abstract：
Pediatric heart transplantation is hampered by a chronic shortage of donor organs. This problem is further confounded by graft rejection. Identification of earlier indicators of pediatric graft rejection and development of subsequent strategies to counteract these effects will increase the longevity of transplanted pediatric hearts. Heart transplant reject is due to a complex series of events, resulting in CAV, which is thought to be mediated through a host immune response. However, the earlier events leading to CAV are not very well known. We hypothesize that early events related to ischemia reperfusion injury during pediatric heart transplantation are responsible for CAV and subsequent graft rejection. Identification of the molecular markers of ischemia reperfusion injury and development of subsequent therapies to block these pathways can potentially lead to a therapeutic strategy to reduce CAV and increase the longevity of the transplanted heart. To accomplish this goal, we have developed a perfusable vascular graft model populated with endothelial cells and demonstrated the feasibility of this model to understand the early events of ischemia reperfusion injury.
摘要：
儿童心脏移植受到供体器官长期短缺的阻碍。这个问题被移植物排斥进一步混淆。识别儿科移植排斥的早期指标以及开发抵消这些影响的后续策略将增加移植儿科心脏的寿命。心脏移植排斥是由于一系列复杂的事件，导致CAV，这被认为是通过宿主免疫反应介导的。然而,导致CAV的早期事件并不是众所周知。我们假设小儿心脏移植过程中与缺血再灌注损伤相关的早期事件是CAV和随后的移植物排斥反应的原因。鉴定缺血再灌注损伤的分子标志物和开发阻断这些途径的后续疗法可以潜在地导致降低CAV和增加移植心脏寿命的治疗策略。为了实现这个目标,我们建立了一个内皮细胞填充的可灌注血管移植模型,并证明了该模型用于了解缺血再灌注损伤早期事件的可行性.
