MOLECULAR PATHWAYS LEADING TO CHRONIC GRAFT DYSFUNCTION

导致慢性移植物功能障碍的分子途径

• 批准号: 8166581
• 负责人: Valeria Raquel Mas
• 金额: $ 0.74万
• 依托单位: VIRGINIA COMMONWEALTH UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-12-01 至 2010-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8166581
• 关键词: Allografting; Atrophic; Biology; Chronic; Chronic rejection of renal transplant; Clinical; Computer Retrieval of Information on Scientific Projects Database; Fibrosis; Functional disorder; Funding; Future; Graft Survival; Grant; Healed; Immunosuppression; Injury; Institution; Kidney; Kidney Transplantation; Molecular; Nephrons; Pathway interactions; Process; Research; Research Personnel; Resources; Series; Source; Survival Rate; Time; Tissues; Tubular formation; United States National Institutes of Health; graft function; healing; improved; interstitial; isoimmunity; kidney allograft; response

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.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 移植肾功能丧失伴肾小管萎缩（TA）和间质纤维化（IF），一组被称为慢性移植物肾病（CAN）的发现，导致大多数移植肾丢失。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。同种异体移植物的持续损伤并不代表一个单一的实体，而是由几种致病性损伤和肾脏愈合反应引起的组织损伤的总和效应，并通过同种免疫和免疫抑制进行修饰。 CAN是对移植肾的一系列时间依赖性损伤的最终结果，导致肾单位的永久性损伤和损失。 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，了解该过程的生物学，并通过发现因果机制来开发治疗方法。