Can Wnt proteins stop atherosclerotic plaques becoming unstable and rupturing?

Regulation of foam cell formation, apoptosis and proliferation by Wnt signalling: implications for atherosclerosis

Professor Sarah Jane George and her team at the University of Bristol have discovered that a family of proteins called Wnt may be important in keeping fatty atherosclerotic plaques stable. When fatty material builds up on the inner lining of arteries and it hardens, an atherosclerotic plaque results. Plaques can become unstable and rupture – if this happens, a blood clot can form and block the narrowed artery, causing a heart attack or stroke if the artery supplying the heart muscle or brain is blocked. Plaques become unstable because inflammatory cells called macrophages within the blood vessel wall take up fat and form foam cells, which cannot be cleared from the plaque. These cells are important for plaque instability but we don’t fully understand how they form and behave. Understanding this process may reveal new ways to prevent atherosclerotic plaques getting more unstable and being at risk of rupture. Professor George and her team have shown that Wnt proteins are particularly abundant in areas of plaques that also have lots of macrophages. They found that Wnt proteins can prevent inflammatory cells taking up fat and becoming foam cells, and can encourage healthy macrophages to survive and grow. Dr George has been awarded a PhD studentship to enable a young scientist to study this process further. The student will determine exactly how Wnt proteins prevent fat uptake and boost macrophage survival. Ultimately, this research could reveal targets for new drugs that could reduce fat uptake by macrophages within the artery, reducing the chances of plaque rupture and ultimately heart attacks and strokes.