Our mission is to understand fundamental mechanisms in molecular and cellular biology leading to cardiovascular diseases.
Current projects and goals
The Vascular Complications Group focuses on the development of atherosclerosis and cardiovascular disease (CVD), with particular emphasis on gene regulation and aberrant cell proliferation and cell death. We have identified a new player in the development of vascular disease; the role of TRAIL (TNF-related apoptosis-inducing ligand) in atherosclerosis and arterial thickening, both in vitro and in vivo using Trail-/- and Trail-/-Apoe-/- mice has already provided critical insights into cell survival and death, in the normal and diseased vessel wall, and opened up new opportunities for therapeutic intervention. Using unique models the Vascular Complications Group’s current research is focused on answering critical questions and exploring underlying mechanisms into vascular diseases, obesity, diabetes and kidney disease.
Comprehension of cellular mechanisms promoting atherosclerosis
This work focuses on the role of blood cells or leukocytes in the development of atherosclerosis. We ask the question “Can we modulating or manipulate the phenotype and function of leukocytes to improve atherosclerosis”. We are also trying to understand the protective abilities of TRAIL during disease.
Finding new ways to promote blood vessel development
This project focuses on the role of TRAIL in ischaemia-induced blood vessel development in vivo. Here we trying to understand the role of endothelial cells and smooth muscle cells in new blood vessel development depend on TRAIL signaling. We are currently comparing outcomes of TRAIL therapy with other therapies currently tested in clinical trials in people for peripheral artery disease.
How is insulin regulated under normal conditions and becomes dysregulated in diabetes?
Indirect evidence suggests that TRAIL regulates insulin expression and secretion. This work focuses on directly assessing whether TRAIL controls insulin expression and secretion at a molecular level, and how/why this is altered during diabetes.