B1a B Cells: Atheroprotective Mechanisms And Therapeutic Application
Funder
National Health and Medical Research Council
Funding Amount
$547,180.00
Summary
Atherosclerosis-related heart attacks and strokes remain leading causes of global deaths despite use of potent lipid-lowering drugs. Thus, another therapeutic option is urgently needed. Our laboratory found that B1a B cells protect against atherosclerosis. We will study the therapeutic efficacy of expanding B1a cells by different approaches in atherosclerosis. Our proposal for clinical translation is to reduce mortality from atherosclerosis-based heart attacks and strokes.
Cardiac Fibrosis In Hypertensive Heart Disease: Cellular And Molecular Mechanism
Funder
National Health and Medical Research Council
Funding Amount
$631,979.00
Summary
Cardiac fibrosis due to excess collagen accumulation in the heart is a major cause of heart failure associated with high blood pressure and greatly increases the risk of sudden death. At present there are no effective therapies to prevent cardiac fibrosis. Understanding how fibrosis develops and identifying the cells and factors responsible will lead to development of novel therapies for cardiac fibrosis.
Regulatory T Cells And Cardiac Fibrosis In Hypertensive Heart Disease: Cellular And Molecular Mechanisms Of Suppression
Funder
National Health and Medical Research Council
Funding Amount
$715,316.00
Summary
Excessive accumulation of collagen in the heart, cardiac fibrosis is a major factor causing heart failure and sudden death. How collagen accumulation occurs in the heart still needs to be elucidated but recent studies in humans and animal models of cardiac fibrosis indicate a significant role for inflammation. The proposed studies are to address this issue and how to regulate inflammation in the heart to suppress cardiac fibrosis, using immune cells called regulatory T cells that suppress inflam ....Excessive accumulation of collagen in the heart, cardiac fibrosis is a major factor causing heart failure and sudden death. How collagen accumulation occurs in the heart still needs to be elucidated but recent studies in humans and animal models of cardiac fibrosis indicate a significant role for inflammation. The proposed studies are to address this issue and how to regulate inflammation in the heart to suppress cardiac fibrosis, using immune cells called regulatory T cells that suppress inflammation.Read moreRead less
Defining The Cellular Basis For Therapeutic Angiogenesis: Characterisation Of Endothelial Progenitor Cell Populations
Funder
National Health and Medical Research Council
Funding Amount
$365,126.00
Summary
Endothelial progenitor cells (EPCs) have been thought to play a role in new blood vessel growth and repair of the heart & blood vessels. Owing to their potential regenerative capacity, there has been immense interest in EPCs as a means of facilitating new blood vessel growth for sufferers of cardiovascular disease. This study will comprehensively evaluate the role of EPCs in new blood vessel formation. It will have implications for potential use of EPCs to treat heart disease.
Defining The Cellular Basis For Therapeutic Angiogenesis: Characterisation Of Endothelial Progenitor Cell Populations
Funder
National Health and Medical Research Council
Funding Amount
$100,943.00
Summary
Cardiovascular disease is the leading cause of death in the Australia. Endothelial progenitor cells (EPCs), similar to stem cells, have strong self-renewal capabilities and the ability to mature further. There has been immense interest in using EPCs as they are believed to have a role in the growth and repair of blood vessels. This research systematically studies two candidate EPCs, the early EPC and the outgrowth EPC (OEC), and potentially paves the way for using EPCs to treat heart disease.
Proatherogenic CD4 NKT Cells And Atherosclerosis: Molecular Mechanisms And Therapeutic Strategies For Suppression
Funder
National Health and Medical Research Council
Funding Amount
$504,348.00
Summary
Immune cells called CD4+ iNKT cells are known to be activated by lipids which initiate development of atherosclerosis, a disorder of blood vessels which is responsible for most heart attacks and strokes. We aim to investigate how these cells contribute to the development of this important blood vessel disoder and examine potential ways of inhibiting their activation to prevent heart attacks and strokes.