New defence mechanism could prevent atherosclerosis

Atherosclerosis is the major cause of death in Australia.  Inflammation and oxidation pathways in the cells that line the coronary arteries lead to the development and progression of this disease. To decrease oxidation and associated inflammation, blood vessel cells have established defence mechanisms. 

We have identified one such mechanism in these cells that involves an enzyme known as DHCR24. This study will determine the reactions promoted by DHCR24 with a view to understanding the molecular events that underpin the protective actions of this enzyme. This information may eventually assist in designing therapies to prevent hardening of the arteries.

Only once we have a fundamental understanding of what processes underlie the development and progression of atherosclerosis will we be in a position to devise effective prevention therapies. 

Sex hormone actions on vascular calcification

The major cause of cardiovascular disease is the build up of fatty lesions in the coronary arteries that eventually get so big they block blood flow to the heart. As we age, these lesions become quite calcified. The more calcified a lesion the more likely the patient will have a cardiovascular event. We are investigating whether hormone replacement therapy affects the rate at which fatty lesions become calcified.

The role of High Density Lipoproteins in regulating new blood vessel growth

For many sufferers of heart disease and cancer, current treatments do not relieve the debilitating symptoms. The growth of new blood vessels can alleviate the effects of a restricted blood supply caused by blocked arteries. Conversely, new vessel growth accelerates some diseases such as cancer. High density lipoproteins (HDLs) are known to protect against the development of heart disease. Recently we identified a beneficial additional role for HDLs in regulating the growth of new blood vessels. This project will investigate the mechanisms for these effects.