As coronary heart disease develops, artery walls thicken. This is partly due to overgrowth of cells in the artery wall. These are covered and supported by a mesh of proteins on the outer surface of the cells.
BHF Professor Andrew Newby studies the breakdown and stability of this protein mesh as a possible target to prevent arterial disease getting worse.
Professor Newby is particularly interested in what happens to the protein mesh in atherosclerosis, the accumulation of fatty plaques in the walls of our arteries.
The mesh can get dismantled by protein-digesting enzymes - called proteases - which can make the plaques unstable and liable to break apart. Rupture of the plaque can trigger a blood clot, which causes a heart attack if it blocks off the blood supply to the heart muscle.
Professor Newby and his team are investigating these underlying mechanisms that make plaques prone to rupture and cause a heart attack.
Who would benefit?
Heart attacks can affect all kinds of people, young and old, and they can have devastating consequences even if a person survives. Apart from the emotional impact of a life-threatening incident, severe and repeated heart attacks can lead to debilitating heart failure.
For Joanne Ward, a post-birth heart attack turned her life upside down. She still has to deal with chest pain, breathlessness and palpitations and she's undergoing tests to see if she needs a heart transplant.
White blood cells
Heart attacks and strokes are often caused by a build up of fatty deposits - called plaques - in the arteries. A specific type of white blood cell enters these plaques to remove the fatty deposits, but these cells can have both harmful and helpful effects on the health of the arteries. The white blood cells produce proteases - some of which make plaques more stable and some of which make plaques more vulnerable.
Professor Newby’s work suggests that chemical signals called cytokines can affect which particular proteases the white blood cells produce and whether they have good or bad effects on plaque stability.
New treatment targets
Professor Newby is now looking to firmly establish whether the chemical signals can drive white blood cells to produce a harmful complement of proteases and cause plaque rupture, or a helpful complement that promotes plaque stability. This could pave the way for new treatments to prevent heart attacks by stopping the harmful activity of white blood cells whilst preserving their helpful activity.
Find out about BHF-funded research into new tests for heart attack diagnosis