Coppinger R J, Baum C L
Department of Human Nutrition and Dietetics, University of Illinois, Chicago 60612, USA.
Nutr Rev. 1999 Sep;57(9 Pt 1):279-82. doi: 10.1111/j.1753-4887.1999.tb01812.x.
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.
动脉粥样硬化之前会出现胆固醇诱导的血管一氧化氮(NO)生成减少以及内皮细胞功能的促动脉粥样硬化性改变。对调节内皮型一氧化氮合酶(eNOS)活性所涉及步骤的仔细剖析表明,胆固醇诱导的小窝蛋白表达通过刺激抑制性小窝蛋白-eNOS复合物的产生来减少NO的生成。