Dr Mary Kavurma

BSc, PhD

Our mission is to understand fundamental mechanisms in molecular and cellular biology leading to cardiovascular diseases.

Dr Mary Kavurma received her PhD in 2003 from the Centre for Vascular Research at The University of New South Wales, Australia. In 2004, she was awarded a CJ Martin Fellowship from the National Health and Medical Research Council (NHMRC) of Australia, to undertake research at the University of Cambridge, UK. In 2007, Mary returned to the Centre for Vascular Research, where she was appointed Group Leader. In 2013, she joined the HRI as Head of the Vascular Complications Group. She is currently a recipient of a Heart Foundation Career Development Fellowship. Mary also has an active interest in promoting medical research to the lay community: her achievements in scientific research, communication and community engagement were acknowledged with a Young Tall Poppy Science Award in 2009.

Current Appointments

Group Leader - Vascular Complications

Heart Research Institute

Fellow

Heart Foundation of Australia

Conjoint Senior Lecturer

The University of Sydney

Conjoint Senior Lecturer

University of New South Wales

Secretary

Australian Vascular Biology Society Committee

Director, SCOLAR

Australian Atherosclerosis Society

Member

Sydney Local Health District Animals Ethics Committe

Dr Mary Kavurma leads group:

Vascular Complications

Research covers areas of:

Prevention & Detection

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Research Project Opportunities

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Vascular calcification

Vascular calcification is increasingly recognised as a problem with aging, in patients with atherosclerosis, as well as in diabetes mellitus and chronic kidney diseases. The pathobiology of vascular calcification is not fully established, and current therapy is linked to preventing disordered bone and mineral metabolism by lowering the circulating levels of both phosphate and calcium. Understanding why and how blood vessels become calcified may lead to the development of new and better therapeutics.

Markers of oxidative stress in atherosclerosis

Atherosclerosis is the most common cause of mortality in the world and a financial burden on healthcare. It is a condition where vascular cells, inflammatory cells, lipids, cholesterol and cellular waste accumulate producing a thickened arterial wall. Oxidative stress is increasingly implicated in the development of atherosclerosis. This project will investigate the gene expression profiles of oxidants and anti-oxidants between diseased and non-diseased arteries, and correlate these with levels of vascular inflammation.

Regulation of insulin

TRAIL is a protein discovered and named with regards to its ability to promote cell death by binding its specific death receptors. It is now recognised that TRAIL signals can also promote non-apoptotic functions such as cell survival, proliferation, migration and differentiation. We recently discovered a novel protective function for TRAIL. In particular, TRAIL-deficient mice not only displayed accelerated atherosclerosis, but also developed features of diabetes e.g. weight gain, adiposity, hyperglycemia and hypoinsulinemia. These suggest that the presence of TRAIL may improve glucose and insulin metabolism. Whether TRAIL regulates insulin expression/secretion directly is unknown. This project seeks to understand how insulin is regulated under normal conditions and dysregulated during diabetes. These studies may lead to improved therapeutics in the treatment of glucose disorders in people.