Vascular endothelial dysfunction is determined by both genetic and environmental factors that cause decreased bioavailability of the vasodilator nitric oxide (NO). This is a hallmark of atherosclerosis, hypertension, and coronary heart disease, which are major complications of metabolic disorders including diabetes and obesity. Excess circulating lipids and glucose that result from disordered metabolism, especially in response to over-nutrition, create a toxic environment that substantially impairs endothelial function. This directly contributes to increased risk for cardiovascular complications and worsening metabolic control. In particular, hyperlipidemia with non-esterified fatty acids (NEFA), lipoproteins, triglycerides and LDL cholesterol promotes increased oxidative stress and pro-inflammatory responses that impair endothelial function and contribute to pro-atherogenic events including thrombosis, and macrophage infiltration. A number of therapeutic interventions, including changes in life style (diet and exercise) as well as pharmacological treatments are useful for improving endothelial dysfunction in the face of lipotoxicity. This review discusses the current understanding of molecular and physiological mechanisms underlying lipotoxicity-mediated endothelial dysfunction as well as relevant therapeutic approaches to ameliorate dyslipidemia and consequent endothelial dysfunction that have the potential to improve cardiovascular and metabolic outcomes.
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|Titolo:||Role of Lipotoxicity in Endothelial Dysfunction|
|Data di pubblicazione:||2012|
|Appare nelle tipologie:||1.1 Articolo in rivista|