Atherosclerosis is preceded by cholesterol-induced diminution in vascular nitric oxide (NO) production and proatherogenic changes in endothelial cell function. Careful dissection of the steps involved in regulating endothelial nitric oxide synthase (eNOS) activity has revealed that cholesterol-induced caveolin expression reduces NO production by stimulating the production of inhibitory caveolin eNOS complexes.
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Coppinger et al. (2009) studied this question.
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