Metabolic syndrome is commonly accompanied by an elevated cardiovascular risk with high morbidity andmortality. The alterations of the arterial vasculature begin with endothelial dysfunction and lead tomicro- and macrovascular complications. The remodeling of the endothelial basal membrane, that promoteserosion and thrombosis, has a multifactorial pathogenesis that includes leukocyte activation, increasedoxidative stress and also an altered matrix metalloproteinases (MMPs) expression. MMPs areendopeptidases which degrade extracellular matrix proteins, such as collagen, gelatins, fibronectinand laminin. They can be secreted by several cells within the vascular wall, but macrophages are determinantin the atherosclerotic plaques. Their activity is regulated by tissue inhibitors of MMP (TIMPs)and also by other molecules, such as plasmin. MMPs could be implicated in plaque instability predisposingto vascular complications. It has been demonstrated that an impaired MMP or TIMP expressionis associated with higher risk of all-cause mortality. A large number of studies evaluated MMPs patternin obesity, diabetes mellitus, arterial hypertension and dyslipidemia, all of which define metabolic syndromeaccording to several Consensus Statement (i.e. IDF, ATP III, AHA). However, few research havebeen carried out on subjects with metabolic syndrome. The evidences of an improvement in MMP/TIMPratio with diet, exercise and medical therapy should encourage further investigations with the intent tocontrast the atherosclerotic process and to reduce morbidity and mortality of this kind of patients.
|Numero di pagine||6|
|Rivista||European Journal of Internal Medicine|
|Stato di pubblicazione||Published - 2012|
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