E-CADHERIN AS A KEY MOLECULE IN RENAL EPITHELIAL-MESENCHYMAL TRANSITION AND FIBROSIS

E-钙粘蛋白作为肾上皮间质转化和纤维化的关键分子

• 批准号: nhmrc : 402435
• 负责人: Prof David Harris
• 金额: $ 21.22万
• 依托单位: The University of Sydney
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2007
• 资助国家: 澳大利亚
• 起止时间: 2007-01-01 至 2008-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/e-cadherin-key-transition-fibrosis/98804
• 关键词: CADHERIN; KEY; MOLECULE; RENAL; EPITHELIAL

Chronic kidney disease (CKD) is a major cause of death and disability in the Australian population. Current treatments for CKD are non-specific and frequently ineffective. As a consequence, kidney failure progresses to the stage where patients require dialysis or transplantation to remain alive. Every year more than 1700 Australians require kidney replacement therapy for this reason and many more die of kidney failure or its complications. Kidney fibrosis is the final common result of diverse CKD. This project proposes to investigate EMT, a key event in the development of renal fibrosis, whereby kidney cells are converted to fibrogenic cells. The project focuses on matrix enzymes (metalloproteinases) and E-cadherin (a molecule which is involved in adherence of kidney cells to one another, but which we think may actually be involved in the causation of EMT). This focus is novel, and could provide new understanding about the process of EMT in renal fibrosis, knowledge relevant to all diseases characterised by eventual loss of organ function due to fibrosis. It will identify new targets for therapy aimed at preventing fibrotic diseases of all types.

慢性肾脏疾病（CKD）是澳大利亚人口死亡和残疾的主要原因。目前CKD的治疗是非特异性的，并且经常无效。因此，肾衰竭进展到患者需要透析或移植才能存活的阶段。每年有超过1700名澳大利亚人因此需要肾脏替代治疗，更多的人死于肾衰竭或其并发症。肾脏纤维化是各种CKD的最终共同结果。该项目提议研究EMT，这是肾纤维化发展中的关键事件，肾细胞转化为纤维化细胞。该项目的重点是基质酶（金属蛋白酶）和E-钙粘蛋白（一种参与肾细胞相互粘附的分子，但我们认为它实际上可能参与EMT的病因）。这一重点是新颖的，可以提供有关肾纤维化中EMT过程的新理解，与所有以纤维化导致器官功能最终丧失为特征的疾病相关的知识。它将确定旨在预防所有类型纤维化疾病的治疗新靶点。