Clare Louise Hawkins
Inflammation, Metabolism and Oxidation
2200 København N.
Clare Hawkins joined the Department of Biomedical Sciences in March 2017, after nearly 20 years in Sydney at the Heart Research Institute, where she held the position of Scientific Director and the Inflammation Group Leader. She is a former Australian Research Council Future Fellow, and Principal Research Fellow within Sydney Medical School, University of Sydney, and has held other prestigious Research Fellowships including an R.D. Wright Career Development Fellowship from the National Health and Medical Research Council of Australia and a Career Development Award from the Australian National Heart Foundation. Her research is focused on understanding the role of oxidative stress and inflammation in driving lesion development in atherosclerosis.
Primary fields of research
Chronic inflammation is the major driving force of the disease atherosclerosis, which is characterised by the accumulation of lipid in infiltrating macrophages in the artery wall. The disease progresses over decades to form complex fatty lesions that lead to the clinical manifestations of myocardial infarction and stroke. The over-production of various chemical oxidants during inflammation and the resulting oxidative stress plays a key role in lesion development. Our research is focused on understanding how oxidants produced during inflammation modify the structure and function of biological molecules and cells associated with the arterial wall. We are also interested in gaining a greater understanding of how immune cell extracellular traps contribute to the development of lesions and other types of disease. Our overall goal is to develop more targeted therapies to prevent lesion formation and slow the progression of atherosclerosis, which might also be relevant to diabetic complications and other types of inflammatory pathologies.
Our group is working to gain a more detailed understanding of how inflammatory oxidants and extracellular traps contribute to the development of disease to allow us to design new strategies to therapeutically target these reactions. Our aim is to develop a treatment to limit damaging reactions to the host during chronic inflammation without compromising innate immune defences.
More details about our projects can be found at the Redox Biology webpage
Understanding the protective mechanisms of selenocyanate in chronic inflammatory disease.
This project investigates a new approach to reduce tissue damage during chronic inflammatory diseases like atherosclerosis without compromising innate immunity.
Examining the role of post-translational histone modification in inflammation.
This project examines the dark side of histones, the nuclear proteins that package DNA but can promote organ failure and death when outside the cell.
Understanding the role of macrophage extracellular traps in disease.
This project investigates a potential new pathway by which macrophages promote lipid accumulation and lesion development in atherosclerosis.
Investigating the role of nucleic acid modification in diabetes and inflammatory disease.
This project examines how the oxidative modification of RNA and DNA perturbs cellular function to promote inflammation, pancreatic islet dysfunction and vascular damage.