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Atherosclerosis is an inflammatory condition and the main cause of CVD, initiated by retention of cholesterol in the vessel wall. Cells of the myeloid lineage, eg, monocytes, macrophages and myeloid-derived suppressor cells, play a pivotal role, either promoting or suppressing atherogenesis, depending on their functional state. The plasticity of these cells creates an opportunity for intervention that may retard or reverse disease progression and prevent acute events. To develop therapeutic strategies, the molecular switches that control myeloid cell function must be identified and characterised. This project seeks to explore functional consequences of several identified proteins that we have shown to control myeloid cell function(s) in atherosclerosis. Using in vivo, ex vivo and in vitro models, we will examine the therapeutic potential of these proteins on atherosclerosis and identify whether manipulating levels will attenuate disease.

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