What is the issue for NSW?
Cardiovascular disease is one of the leading causes of death in NSW. Rates of chronic kidney disease are increasing exponentially in NSW compared to the rest of Australia, and 11% of the population is affected by diabetes mellitus. The most common reason for hospital admission in NSW is care involving renal replacement therapy (dialysis) for kidney failure.
Patients with chronic kidney disease also experience significantly reduced life expectancy due to cardiovascular (heart) disease. Our understanding of the biology underlying heart disease – and how it is worsened by kidney failure and diabetes – is also limited, which is delaying development of specific drugs and markers of disease.
This proposal identifies a new molecule driving heart disease, facilitating development of therapeutics to improve quality of life, lower mortality rates and reduce healthcare costs.
What does the research aim to do and how?
The overarching goal of this project is to define how diabetes and chronic kidney disease modulate the cardiovascular pathology, particularly cardiac remodelling and atherosclerosis. This research will investigate the contribution of a new molecular pathway that regulates matrix protein expression in all three conditions, and how limiting signalling can reduce development of cardiovascular disease through comparison with current standard of care.
This research provides a strong health benefit by identifying a novel molecular target for diabetic cardiorenal syndrome and testing new therapeutics to reduce disease in a strong pre-clinical model, which have potential clinical applications in a condition with limited treatment options.
The top three key measures/indicators being used to assess the research outcomes are:
- Understand how cells in the heart and blood vessels change in response to diabetes and kidney disease.
- Investigate how a protein can change plaque core size and/or cap thickness which alters the risk of rupture.
- Develop a new treatment that reduces heart remodelling and plaque burden.