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Role Of JNK And P38 MAPK Signalling In Diabetic Nephropathy
Funder
National Health and Medical Research Council
Funding Amount
$454,500.00
Summary
Renal failure is a major health problem in our community. Patients who progress to end-stage renal failure are dependent upon lifelong dialysis or transplantation (an expensive and complex treatment). The past decade has seen a dramatic increase in the number of patients developing end-stage renal failure, mainly due to increasing rates of diabetic kidney disease. Indeed, the recent AusDiab nationwide survey that identified diabetes or glucose intolerance (a precursor to diabetes) is now present ....Renal failure is a major health problem in our community. Patients who progress to end-stage renal failure are dependent upon lifelong dialysis or transplantation (an expensive and complex treatment). The past decade has seen a dramatic increase in the number of patients developing end-stage renal failure, mainly due to increasing rates of diabetic kidney disease. Indeed, the recent AusDiab nationwide survey that identified diabetes or glucose intolerance (a precursor to diabetes) is now present in up to 25% of the adult Australian population. Around 50% of diabetics develop kidney disease and, despite recent advances in better control of blood glucose and blood pressure, kidney disease in most diabetic patients will inexorably progress to end-stage renal failure. Therefore, there is an urgent need to improve treatment strategies in diabetic patients to avoid kidney failure. We have identified a group of proteins (enzymes called JNK and p38) within cells that play a causal role in the development of non-diabetic forms of kidney disease. Most recently, we have shown that an increase in the activity of these proteins (JNK and p38) is associated with the development of human and experimental diabetic kidney disease. Therefore, this project will block the action of JNK and p38 using two complementary approaches (pharmaceutical drugs and genetically modified mice) to determine whether targeting these proteins can suppress the development of diabetic kidney disease. In addition, there is evidence to suggest that blockade of these proteins may have a beneficial impact upon insulin resistance and elevated blood glucose in type 2 diabetes. If these postulates are proven, this will provide a well-defined therapeutic target for the treatment of diabetic kidney disease, and perhaps diabetes itself. Furthermore, since inhibitors of these proteins are already in clinical trials for other indications, targeting this mechanism in diabetic kidney disease is a realistic goal.Read moreRead less
Apoptosis Signal-regulating Kinase 1 (ASK1) Is A Major Pathway Of Stress-induced Renal Injury In Different Types Of Progressive Kidney Disease.
Funder
National Health and Medical Research Council
Funding Amount
$678,865.00
Summary
Oxidative stress plays an important role in progressive kidney disease. We have identified a stress-activated mechanism (the ASK1 pathway) through which oxidative stress may cause kidney disease. We will perform preclinical studies in models of different types of kidney disease with an ASK1 inhibitor drug and genetically modified mice. These studies will provide new insights into the pathogenesis of kidney disease and will determine the potential of ASK1 as therapeutic target in kidney disease.
Selective Targeting Of Acute Renal Injury By Inhibition Of The Receptor Tyrosine Kinase, C-fms.
Funder
National Health and Medical Research Council
Funding Amount
$443,007.00
Summary
The progression of kidney disease to end-stage renal failure is a major health problem in our community. We have identified that macrophages, a type of white blood cell, plays an important role in causing inflammatory kidney injury. This project will use clinically relevant animal models to test the therapeutic potential of our new approach to selectively remove these cells from the inflamed kidney and thereby protect it from injury.