Atherosclerosis and Metabolic Syndrome-significance of Inflammation, Urgency of Weight Loss and Extracorporeal Removal of Proinflammatory and Proatherogenic Substances

Abstract

The link between atherosclerosis and metabolic syndrome is through system inflammation. Molecular mechanisms of this link can be explained by hypothesis that arterial hypertension, central obesity and insulin resistance are connected through dysfunction of endothelium and inflammation, where major role play tumor necrosis factor alpha (TNF-a) and reactive oxygen species (ROS), that promotes modulation of insulin receptor substrare2 (IRS2) signaling, insulin resistance, nuclear factor NF-kB (NF-kB) and IκB kinase β activation, endothelial dysfunction, oxidized low density lipoproteins accumulation, vascular inflammatory responses with vascular smooth muscular cells apoptosis and atherosclerotic plaque instability. TNF-a and ROS overproduction closely linked with central obesity and adipocytokines deregulation. Morphological substrate of atherosclerosis-plaque, it’s stability and evolution depends on intensity proinflammatory mediators and matrix metalloproteinases production, that closely bind with metabolic syndrome components, such as central obesity with adipocytokines production; arterial hypertension with endothelial dysfunction; glucose intolerance, insulin resistance and its intracellular signaling disturbances; oxidized low density lipoproteins accumulation and oxidative stress.