Differential effects of elevated cholesterol and fatty acids on endothelial function: Mechanisms contributing to atherosclerosis development

The impairment of endothelial function occurs through LDL cholesterol and saturated/ trans fatty acids which cut down NO production while rising ROS levels and starting NF-κB signaling processes. The activity of glycolysis becomes blocked because palmitic acid triggers PKM2-C31 palmitoylation which leads to increased damage. Among the tested fats trans fats elaidic and linoelaidic created the most damaging oxidative reactions. The monounsaturated fat oleic acid promoted both elevated NO production and decreased inflammation in cells. Thus, we show that different lipids activate unique biological mechanisms toward the production of atherosclerosis.