Identifying critical mechanisms in the initiation of atherosclerosis
Professor Peter Weinberg (lead researcher)
Imperial College London
Start date: 01 September 2011 (Duration 5 years)
Identifying critical mechanisms in the initiation of atherosclerosis
Atherosclerosis develops when fatty deposits build up in the walls of arteries narrowing them and thus reducing the amount of blood reaching organs. If a fatty plaque ruptures it can block the artery and cause a heart attack or stroke. We know that atherosclerosis affects some regions of our arteries more than others, but we don’t know why. It’s possible that variation in blood flow in different parts of the arteries and differences in the way the cells in the artery walls take up large molecules such as ‘harmful’ – LDL – cholesterol may play a role. Areas of an artery affected by atherosclerosis change with age and Professor Peter Weinberg, at Imperial College London, has shown that the uptake of large molecules by the wall changes with age in a similar way. Professor Weinberg believes that age related changes are caused by changes in the way molecules are transported across the endothelium – the lining of the artery wall. In this programme he will carry out detailed studies, using rabbits at various ages, to identify patterns of atherosclerosis and pinpoint areas of the artery walls where large molecules are taken up more readily. He will also determine how these patterns are affected by changes in mechanical stresses and strains on the arteries, and look for other underlying causes. The research builds on ongoing collaborations between engineers and biomedical experts at Imperial College’s BHF Centre of Research Excellence. Understanding exactly what drives atherosclerosis will help scientists devise novel methods to control it, and may in future help prevent disease.
Project details
Grant amount | £1,340,693 |
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Grant type | Chairs & Programme Grants |
Application type | Programme Grant |
Start Date | 01 September 2011 |
Duration | 5 years |
Reference | RG/11/5/28743 |
Status | Complete |