Regulation, consequences and treatment of mitochondrial dysfunction in atherosclerosis
Mitochondria are powerhouses of cells that provide energy for all its functions. In atherosclerosis, where fatty plaques have started to form in blood vessels, mitochondria do not work properly. This prevents the waste removal processes that rid the body of dead cells from occurring, causing a build-up of dead tissue (called the necrotic core) and scar tissue (called the fibrous cap) within the plaque. Plaques that have these features are more likely to rupture and move around the body, which can cause a blockage that leads to heart attack or stroke. Dr Yu wants to understand exactly how mitochondria affect the removal of dead cells in plaques by another type of cell called a macrophage. She is focusing on a protein called tafazzin. Dr Lu will investigate how tafazzin affects mitochondrial function in blood vessel cells, macrophages and in mice with atherosclerosis. She will then test whether a drug that targets tafazzin can stabilise atherosclerotic plaques in the mice. The final part of the study will investigate a link between tafazzin levels and the stability of human atherosclerotic plaques. Together, the results could lead to treatments to prevent plaque rupture, reducing the chance of heart attack or stroke.
Project details
| Grant amount | £1,037,352 |
|---|---|
| Grant type | Fellowships |
| Application type | Intermediate Clinical Research Fellowship |
| Start Date | 01 June 2019 |
| Duration | 5 years |
| Reference | FS/19/2/34017 |
| Status | In Progress |
