Atherosclerotic plaques are fatty, cellular lesions that form in artery walls. They are the most common cause of heart attacks and strokes. Plaques contain immune cells called macrophages that are recruited to ingest and remove lipids (“bad cholesterol”) that have entered from the bloodstream. Ineffective lipid removal, due to macrophage death and other factors, leads to the accumulation of dead material and lipid-loaded macrophages. Lipid loading can dramatically alter macrophage functionality, which has implications for plaque fate. Recent work by myself and others has pioneered the development of lipid-structured models to study macrophage population dynamics during atherosclerotic plaque growth. In this talk, I will discuss these models and highlight some of the novel insights they have provided. As well as opening a new window on plaque formation, these models are mathematically interesting entities. They are formulated as advective partial integro-differential equations with positive and negative non-local advection terms that account for macrophage efferocytosis (dead cell consumption) and proliferation (live cell division).
Zoom link: https://uni-sydney.zoom.us/j/86189644574?pwd=OUpzdXhScW5XNVo0Z0xaamE2VS9EUT09
Passcode: 620652

School Seminar Series: 


Michael Watson




Thu, 17/03/2022 - 11:00am


Online (see abstract for Zoom link and passcode)