Our objective
Our mission is to understand the contribution of specific oxidative processes to the formation of unstable atherosclerotic plaque. We aim to understand the mechanisms and factors that distinguish formation of unstable versus stable plaque, and how this knowledge can be used to selectively identify and treat unstable plaque.
Our impact
Atherosclerosis is the main underlying cause of cardiovascular diseases such as heart attack and stroke. It is very common – people over the age of 40 have an approximately 50 per cent chance of developing serious atherosclerosis, with this risk increasing with age.
There are two types of atherosclerotic plaques: stable and unstable. Stable plaques can be identified and treated readily. In contrast, there is currently no reliable and non-invasive method to identify unstable plaque, yet the rupture of such plaques is thought to cause 30-50 per cent of all fatal heart attacks. Understanding the mechanism of formation of unstable plaque could pave the way for the development of new methods to identify and eventually treat high-risk unstable plaque, thereby saving lives and providing a better health outcome for the millions around the world who have atherosclerosis.
Collaborators
Professor Rene Botnar, King’s College, London
Professor David Celermajer, HRI Clinical Research Group
Prof Catherine Clarke, University of California
Prof Ian Dawes, University of New South Wales
Professor Philip Eaton, Queen Mary University London
Dr Mary Kavurma, HRI Vascular Complications Group
Prof Tony Kettle, University of Otago
Dr Ashish Misra, HRI Atherosclerosis and Vascular Remodelling Group
Assoc Prof Sanjay Patel, HRI Coronary Diseases Group
Dr Imran Rashid, University Hospitals Cleveland
Professor Christine Winterbourn, University of Otago
Selected publications
Stanley CP, et al. Singlet molecular oxygen regulates vascular tone and blood pressure in inflammation. Nature 2019;566 (7745), 548–552.
Talib J, et al. A concurrent multi-omics method to assess metabolic changes associated with atherosclerosis using small amounts of arterial tissue from a single mouse. Analytical Chemistry 2019;91:12670-12679.
Cheng D, et al. Inhibition of MPO (myeloperoxidase) attenuates endothelial dysfunction in mouse models of vascular inflammation and atherosclerosis. Arteriosclerosis, Thrombosis and Vascular Biology 2019;39:1448-1457.
Rashid I, et al. Myeloperoxidase is a potential molecular imaging and therapeutic target for the identification and stabilization of high-risk atherosclerotic plaque. European Heart Journal 2018;39 (35), 3301–3310.
Stocker R, Keaney Jr JF. Role of oxidative modifications in atherosclerosis. Physiological Reviews 2004;84 (4), 1381–1478.
Stocker R, et al. Bilirubin is an antioxidant of possible physiological importance. Science 1987;235 (4792), 1043–1046.