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Title: Metabolic syndrome and atherosclerosis: the role of oxidative stress and inflammation
Authors: Eugenia Hopps
Affiliations: Department of Emergency Medicine, University Hospital of Palermo ia del Vespro, Palermo 129 - 90127, Italy.
Abstract: Metabolic syndrome (MS), which involves factors as obesity, insulin resistance, diabetes mellitus, arterial hypertension and dyslipidemia, is commonly accompanied by an elevated cardiovascular risk with high morbidity and mortality. The alterations of the arterial vasculature begin with the endothelial dysfunction and lead to micro- and macrovascular complications. The remodelling of the endothelial basal membrane, which promotes erosion and thrombosis, has a multifactorial pathogenesis that includes leukocyte activation, subclinical inflammation, increased reactive oxygen species (ROS) production, and also an altered matrix metalloproteinases (MMPs) expression.
A strong association between MS and an altered oxidant/antioxidant status has been demonstrated. In case of endothelial dysfunction, the superoxide anion oxidizes nitric oxide (NO) reducing its availability and starting a cascade of ROS generation that leads to the oxidation of carbohydrates, proteins and lipids. Oxidized low-density lipoproteins (oxLDLs) are often increased in newly diagnosed MS subjects.
MMPs are endopeptidases degrading extracellular matrix proteins, which are involved in the atherosclerotic lesion development and progression and could be implicated in plaque instability. In MS an impaired MMP expression has been demonstrated and it is associated with a higher risk of all-cause and cardiovascular mortality.
Chronic systemic inflammation is a common feature of MS, and it is mostly induced by the release of inflammatory molecules (IL-6, TNF-α, leptin, adiponectin, resistin) in the visceral adipose tissue. The proinflammatory status seems to be the link between oxidative stress and MMP profile in MS and it contributes to the plaque development influencing the activity of endothelial cells, macrophages and vascular smooth muscle cells.