Cardiovascular Disease (CVD) encompasses a number of conditions such as coronary heart disease, stroke, arrhythmias, aneurysm and peripheral vascular disease amongst others. It is the leading cause of death worldwide, being responsible for 17.3 million deaths (31.5% of all deaths) in 2013.
Atherosclerosis is the leading cause of death from heart attack and stroke, contributing to 75% of deaths from CVD. Hypertension is a major risk factor for most CVDs and also for chronic kidney disease.
While the risk of developing a heart attack or stroke can be reduced through lifestyle modifications there is a great need for much more effective approaches to CVD prevention and treatment. For example, the aetiology of most cases of adult hypertension is unknown, treatment-resistant hypertension is common and this disease remains a public challenge. For stroke, there are no effective drug treatments besides clot lysis that must be administered within 4 1/2 hours, thus excluding approximately 90 % of victims. Across CVD indications, the failure rate of new drug candidates is high and there is a need to identify new biomarkers and develop improved and targeted treatments.
There is also a strong association between heart health/disease and kidney health/disease - most patients with kidney disease die from CVD and, on the other hand, kidney disease impacts in a major way on heart health. There is a high unmet need for treatments to prevent or slow progression of kidney diseases.
Who we are
Professor Kate Denton leads our CVD program, which comprises 9 group leaders and their research teams, as well as 15 group leaders from other BDI programs such as such as Metabolism, Diabetes and Obesity. The collective expertise traverses several domains of CVD research, bringing critical mass to the areas of stroke and hypertension, atherosclerosis, fibrosis and kidney disease. Interactions across programs lend a cross-disciplinary approach in alignment with overlap in disease areas.
Our research will inform on the basic principles of the cardiovascular system from cell biology through to organ systems such as the role of brain, heart, kidney, lung and vasculature in health and disease. Ultimately, we seek to improve the health of our ageing population by reducing the burden of chronic cardiovascular diseases (hypertension, atherosclerosis) and the resulting major cardiovascular events (myocardial infarction, stroke). Our researchers are working to further our understanding of the cardiovascular system in health and disease with the aim to identify novel therapeutic targets to treat a range of CVDs. Some important questions we seek answers to include:
- Can we identify therapies that treat the causes and not just the symptoms of CVD?
- How does the immune system contribute to chronic CVD?
- How do different organs interact in the progression of CVD?
- Can we refine risk factor assessment to better identify patients at risk of a cardiovascular event?
- What experimental CVD models are needed to support translation?
- How do the risk factors for chronic CVD in the rural poor in low-to-middle income countries differ from those in developed nations?
Our researchers have extensive expertise across several overlapping research themes. The core areas of enquiry include:
We are exploring the disease mechanisms that cause essential hypertension using experimental models that appear to be predictive of the hypertensive state in humans. We seek to clarify whether hypertension is an autoimmune disease and whether we can therapeutically target the immune system to treat patients that do not respond to conventional therapies. An important treatment pathway under extensive investigation for providing better blood pressure control is the manipulation of the renin-angiotensin system.
Our research is directed towards finding better treatments by identifying and then targeting the complex mechanisms of primary and secondary brain injury, systemic consequences of stroke, as well as promotion of healing and functional recovery through cell-based therapies.
Fibrosis and atherosclerosis
Our focus is to identify how to detect and stabilise rupture-prone plaques to prevent heart attack and stroke events. This involves the discovery of new biomarkers and development of imaging techniques to detect collagen deposition and rupture prone plaques. For the prevention and treatment of organ fibrosis we are exploring whether the promotion of an anti-inflammatory M2 macrophage phenotype stabilises atherosclerotic plaques and whether novel NO-based drugs confer protection in the setting of atherosclerosis.
We are investigating the key role of renal hypoxia in the pathogenesis of acute and chronic kidney disease, and how this can lead to new treatments. We are also developing methods of monitoring kidney health in critically ill patients and investigating how we can prevent acute kidney injury in critically ill patients in a hospital setting.