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Circulating Low -molecular Weight AGEs In The Development And Progression Of Diabetic Complications
Funder
National Health and Medical Research Council
Funding Amount
$297,523.00
Summary
High levels of sugars seen in patients with diabetes leads to damage of many organs including the heart, the eyes and the kidneys. These high sugars cause damage through a number of mechanisms, one being the formation of advanced glycation end products or AGEs, formed by the irreversible reaction between proteins and glucose. This reaction leads to a change in the shape and function of AGE-modified molecules that progressively contributes to organ damage. AGEs also bind and activate specific rec ....High levels of sugars seen in patients with diabetes leads to damage of many organs including the heart, the eyes and the kidneys. These high sugars cause damage through a number of mechanisms, one being the formation of advanced glycation end products or AGEs, formed by the irreversible reaction between proteins and glucose. This reaction leads to a change in the shape and function of AGE-modified molecules that progressively contributes to organ damage. AGEs also bind and activate specific receptors that promote the damage and scarring of tissue. Where the glucose concentration is high, AGEs accumulate much more quickly. This is one reason why patients with good sugar control do better than those who are unable to control their blood sugars. The importance of this AGE pathway is illustrated by the fact that blocking the formation of AGEs is able to prevent kidney damage in animals with diabetes. In addition, exposure to AGEs can cause diabetes-like changes in the absence of high sugars. Our laboratory is a world leader in the study of the advanced glycation and methods blocking this process. The research proposed will investigate circulating levels of AGEs in experimental animals and patients with diabetes, and correlate them with the development and progression of complications of diabetesRead moreRead less
We have validated CDA1 as an effective target to retard kidney disease in diabetes using a mouse model where we deleted the CDA1gene. We have also developed a novel agent to inhibit CDA1 in order to retard diabetic kidney disease. In this application, we propose to confirm the efficacy of targeting CDA1 using various diabetes models and a range of strategies to target CDA1. We will also rigorously explore translation of these findings to a new treatment for diabetic renal disease.
Role Of Growth And Transcription Factors In Tubulointerstitial Injury In Diabetes
Funder
National Health and Medical Research Council
Funding Amount
$454,023.00
Summary
Progressive kidney disease occurs as a result of a range of molecular and cellular pathways. One of the commonest causes of kidney disease is diabetes and this appears to be partly related to increased expression and action of certain growth factors such as CTGF. These factors promote the deposition of scar tissue in the kidney and one of the ways these promote this scarring is to change a cell s behaviour so that it now lays down collagen. This proposal will not only focus on how CTGF promotes ....Progressive kidney disease occurs as a result of a range of molecular and cellular pathways. One of the commonest causes of kidney disease is diabetes and this appears to be partly related to increased expression and action of certain growth factors such as CTGF. These factors promote the deposition of scar tissue in the kidney and one of the ways these promote this scarring is to change a cell s behaviour so that it now lays down collagen. This proposal will not only focus on how CTGF promotes scarring but will explore 2 novel factors called Snail and Slug which can act directly on particular genes such as CTGF to inhibit these deleterious effects. By further characterising these pathways involving Snail, Slug and CTGF in the kidney it will be possible to generate new targets and therapies for various forms of progressive kidney disease including diabetic kidney disease.Read moreRead less
In various kidney diseases including the most common cause of end stage kidney disease, diabetic nephropathy, identifying the molecular mechanisms responsible for kidney failure will greatly assist in defining new therapeutic targets in order to develop new treatments and therapies. The studies described in this proposal highlight the involvement of a novel class of small RNA molecules, and provide us with a novel approach to tackle this disease.
Kidney fibrosis is a serious complication seen in diabetic subjects. This process is mainly controlled by transforming growth factor beta (TGF-beta). However, direct targeting of TGF-beta as a therapeutic approach is inappropriate due to its other important functions. Our preliminary data show that Cell Division Autoantigen 1 (CDA1) is critical for the disease causing activity of TGF-beta. We propose to use our recently generated unique CDA1 gene knockout mouse to demonstrate this important role ....Kidney fibrosis is a serious complication seen in diabetic subjects. This process is mainly controlled by transforming growth factor beta (TGF-beta). However, direct targeting of TGF-beta as a therapeutic approach is inappropriate due to its other important functions. Our preliminary data show that Cell Division Autoantigen 1 (CDA1) is critical for the disease causing activity of TGF-beta. We propose to use our recently generated unique CDA1 gene knockout mouse to demonstrate this important role of CDA1.Read moreRead less
Fibrosis is a major mechanism driving chronic disease. A specific pathologic process (TGF/Smad signalling) plays an important role in scarring of the kidney and the heart; but our understanding of this process is limited. Our exciting new data has identified a chemical modification of a component of this scarring pathway (acetylation of Smad3), and this project seeks to determine whether this modification plays a pivotal role in regulating tissue scarring.
Cell Type Specific Mechanisms Of Mineralocorticoid Mediated Renal Injury In Glomerulonephritis And Diabetic Nephropathy
Funder
National Health and Medical Research Council
Funding Amount
$103,582.00
Summary
Mineralocorticoid exists normally in the human body to maintain fluid and salt balance. However, it is also implicated in diseases affecting the heart and the kidneys. My research aims to further our understanding on how mineralocorticoids contribute to kidney disease, and in particular, to investigate the role of specific kidney cells on mediating kidney injury. Ultimately this research may facilitate development of treatments allowing cell specific blockade of mineralocorticoids, which may red ....Mineralocorticoid exists normally in the human body to maintain fluid and salt balance. However, it is also implicated in diseases affecting the heart and the kidneys. My research aims to further our understanding on how mineralocorticoids contribute to kidney disease, and in particular, to investigate the role of specific kidney cells on mediating kidney injury. Ultimately this research may facilitate development of treatments allowing cell specific blockade of mineralocorticoids, which may reduce kidney diseases such as diabetic nephropathy.Read moreRead less
Mineralocortioid Receptor-Mediated Injury In Progressive Kidney Disease
Funder
National Health and Medical Research Council
Funding Amount
$707,008.00
Summary
Diabetes is the major cause of kidney failure. Activation of a hormone receptor (the mineralocorticoid receptor-MR) can promote kidney injury. Current drugs blocking MR can suppress diabetic kidney disease but are limited by their poor specificity and harmful side effects. Our study will help improve strategies for blocking MR by identifying the cell types responsible for MR-mediated injury and by examining whether a new class of drug targeting MR is a superior therapy to current MR inhibitors.