Atherosclerosis is a leading cause of death worldwide.
Atherosclerotic plaque or atheroma consist of smooth muscle cells (SMCs) and macrophages in the malefactor lesion and are comprised of a lipid-laden core covered by a fibrous cap. Plaque rapture leads to thrombosis with dire consequences, such as myocardial infarction and stroke.
SMCs and macrophages are key players in atherogenesis. Although extensive research has been done in the past on atherosclerosis, exactly how cells from the normal blood vessel wall contribute to the atherosclerotic plaque cap is still far from clear. Our studies aim to discover the origin of the cells that make normal blood vessels and how these cells contribute to atherogenesis.
Recently, our studies established that very few SMCs have the potential to migrate and proliferate from the blood vessels and produce most of the SMCs in atherosclerotic plaques. The focus of our current studies is to identify new signalling molecules, factors and/or pharmacological inhibitors that can modulate SMC phenotypic switching and macrophage infiltration into the plaque to change the plaque composition and thereby promote plaque stability.