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.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 肾移植功能丧失肾脏萎缩（TA）和间质纤维化（如果），一组称为慢性同种异体移植肾病（CAN）的发现会导致大多数肾脏同种异体移植物损失。尽管在免疫抑制方面取得了进展，但仍可以是提高长期移植生存率的主要临床挑战。对同种异体移植的持续损害并不代表单个实体，而是几种致病性损伤的组织损伤的汇总作用以及通过同种免疫和免疫抑制修饰的肾脏的愈合反应。 CAN是对移植肾脏的一系列时间依赖性侮辱的最终结果，导致了永久性损害和肾脏的损失。 肾脏移植未来的一个主要挑战是确定罐头的独特和可识别的原因，了解过程的生物学，并通过发现因果机制来开发治疗方法。