MOLECULAR PATHWAYS LEADING TO CHRONIC GRAFT DYSFUNCTION

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 移植肾功能丧失伴随肾小管萎缩(TA)和间质纤维化(IF)，这是一组被称为慢性移植物肾病(CAN)的发现，是导致大部分移植肾丢失的原因。尽管在免疫抑制方面取得了进展，但CAN仍然是提高移植物长期存活率的主要临床挑战。对同种异体移植物的持续损伤并不代表单一的实体，而是几种病原性侮辱造成的组织损伤和肾脏的愈合反应的总和，经同种异体免疫和免疫抑制修改。 CAN是对移植肾脏的一系列随时间变化的侮辱的最终结果，导致永久性损害和肾单位的丧失。肾移植未来的一个主要挑战是确定CAN的独特和可识别的原因，了解这一过程的生物学过程，并通过发现病因机制来开发治疗方法。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Loss of kidney graft function with tubular atrophy (TA) and interstitial fibrosis (IF), a set of findings termed chronic allograft nephropathy (CAN), causes most kidney allograft losses. Despite progress in immunosuppression, CAN remains the main clinical challenge for improving long-term graft survival rate. The sustained damage to the allograft does not represent a single entity, but the summated effects of tissue injury from several pathogenic insults and the kidney's healing response, modified by alloimmunity and immunosuppression. CAN is the end-result of a series of time-dependent insults to the transplanted kidney resulting in permanent damage and loss of nephrons. A major challenge in the future of kidney transplantation is to identify the distinct and identifiable causes of CAN, to understand the biology of the process, and to develop treatments through the discovery of causal mechanisms.