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

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，而且常常无效。结果，肾衰竭发展到病人需要透析或移植来维持生命的阶段。每年有1700多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。肾纤维化是多种慢性肾病的最终共同结果。本项目拟研究EMT，这是肾纤维化发展中的一个关键事件，肾细胞由此转化为纤维化细胞。该项目侧重于基质酶（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与EMT的病因有关）。这一焦点是新颖的，可以提供关于肾纤维化中EMT过程的新认识，以及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。它将确定新的治疗目标，旨在预防所有类型的纤维化疾病。

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.