Cholesterol Trafficking

About

About Coronary Heart Disease (CHD) is the UK's biggest killer with an average of 200 deaths every day. The principal cause of CHD is atherosclerosis, the accumulation of cholesterol within fatty deposits on the artery walls. Removal of excess cholesterol from macrophages within the arterial wall is a key therapeutic goal, potentially capable of regressing and/or stabilising the development of atherosclerotic lesions. Researchers at Glasgow Caledonian University are investigating the targeting of mitochondrial cholesterol trafficking in macrophages via a translocator protein (TSPO). TSPO can increase the generation of ligands and expression of sterol-sensitive transcription factors controlling the production of proteins mediating the anti-atherogenic cholesterol efflux pathway. Drugs which target this protein may therefore be able to help the body remove atherosclerotic plaque on arterial walls. Drugs which lower the amount of cholesterol in the bloodstraem are widely available (statins), however there are currently no drugs available which can reverse the accumulation of fatty deposits in arteries. Key Benefits TSPO is induced in human atherosclerotic lesions, providing an attractive target for drug therapy. Targeting TSPO avoids the induction of endogenous lipid biosynthesis, a side-effect with some existing drugs that activate the cholesterol efflux pathway. Small molecules targeting TSPO are already in development for other disease conditions. Applications Modulation of cellular cholesterol content in a number of disease conditions, notably coronary heart disease. Potential use as a diagnostic test for susceptibility/pre-disposition to coronary heart disease. IP Status The technology is protected by a patent application. The University welcomes contact from organisations who are interested in discussing collaboration or co-development to further investigate use of TSPO in the modulation of cellular cholesterol efflux.