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Two models describe early events initiating atherosclerotic plaque formation, whereby foam cells form in response to hyperlipidaemia or inflammation\u2010associated stimuli. Although these models are inextricably linked and not mutually exclusive, identifying the unique contribution of each in different disease settings remains an important question. Circulating monocytes are key mediators of atherogenesis in both models as precursors to lipid\u2010laden foam cells formed in response to either excess lipid deposition in arteries, signalling via pattern\u2010associated molecular patterns or a combination of the two. 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