Abstract
Abstract Atherosclerosis is well recognised as a disease associated with elevated cholesterol levels. Innate monocytes and macrophage cells laden with cholesterol have long been described as key players in driving low grade inflammation characteristic of atherosclerosis. In more recent times it has been shown how various mechanisms controlling metabolic and epigenetic reprogramming of these innate immune cells influence their inflammatory responses. In this review a general role of intracellular metabolism in reprogramming innate immune cells will be discussed with a particular emphasis on evidence supporting how innate reprogramming contributes to the pathophysiology of atherosclerosis. In addition the evidence for the role of statins in altering these metabolic adaptations to control the development and progression of atherosclerotic plaques is discussed.
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