How does a protein called SIRT1 prevent harmful blood clot formation?

SIRT1: A novel antithrombotic target in cardiovascular disease?

Heart attacks and strokes occur when blood clots form and block the blood supply to the heart or brain. When blood vessels are damaged, small blood cells called platelets are activated and clump together to form a clot. In healthy blood vessels, many processes occur that prevent platelets from being activated and forming clots unnecessarily. For example, signals within platelets dampen down their responses, and signals from cells that line the blood vessels – endothelial cells – make it harder for platelets to stick together. In diseased blood vessels, platelets are more prone to being activated and forming clots, increasing the risk of a heart attack or stroke. Reduced levels of an important protein called SIRT1 are associated with heart and circulatory disease and type 2 diabetes. Dr Jones has shown that SIRT1 is present in platelets and prevents them from sticking together. Dr Jones will now supervise a project to investigate how, and to what extent, SIRT1 dampens down platelet activity. Researchers will study human stem cells, coronary artery endothelial cells, and blood samples to determine the role of SIRT1 in platelet formation, platelet function, and clot formation. The effects that molecules that activate SIRT1 have on the anti-clotting action of endothelial cells will also be investigated. If the effects are beneficial, molecules that activate SIRT1 could be introduced as new anti-clotting treatments to protect people against heart attacks and strokes.