Professor Andrew Newby

BHF Chair of Vascular Cell Biology

University of Bristol, Bristol Heart Institute

As coronary heart disease 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.

Professor Newby studies the breakdown and stability of this protein matrix as a possible target to prevent disease progression.

Heart attacks

Professor Newby is particularly interested in what happens to the protein matrix in atherosclerosis, the accumulation of fatty plaques in the walls of our arteries.

The matrix 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.

White blood cells

Certain white blood cells called macrophages enter plaques to remove the fatty deposits, but these cells can have both harmful and helpful effects on the health of the arteries. Macrophages 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 macrophages produce and hence whether they have good or bad effects on plaque stability.

New treatment targets

Professor Newby is now looking to firmly establish whether cytokines can indeed drive macrophages 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 selectively modifying the harmful activity of macrophages whilst preserving their helpful activity.