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The earliest manifestation of atherosclerosis at the arterial cell level is lipid accumulation and foam cell formation driving by modified LDL. ER stress promotes macrophage-derived foam cell formation by up-regulating of scavenger receptors, which interact with modified LDL like oxLDL. Whereas, receptors to HDL are down-regulated by the ER stress and the efflux becomes less effective.

In normal macrophages, low density lipoprotein (LDL) cholesterol particles are loaded from late endosomes to the ER. In the ER, cholesterol is esterified and accumulates to form inert lipid droplets. In atherosclerotic macrophages, ER-mediated cholesterol reesterificationis markedly reduced or failed resulting in heavy intracellular deposits of nonesterifiedcholesterol in foam cell.)