Matrix metalloproteinases in metabolic syndrome

Metabolic syndrome is commonly accompanied by an elevated cardiovascular risk with high morbidity and mortality. The alterations of the arterial vasculature begin with endothelial dysfunction and lead to micro- and macrovascular complications. The remodeling of the endothelial basal membrane, that promotes erosion and thrombosis, has a multifactorial pathogenesis that includes leukocyte activation, increased oxidative stress and also an altered matrix metalloproteinases (MMPs) expression. MMPs are endopeptidases which degrade extracellular matrix proteins, such as collagen, gelatins, fibronectin and laminin. They can be secreted by several cells within the vascular wall, but macrophages are determinant in 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 predisposing to vascular complications. It has been demonstrated that an impaired MMP or TIMP expression is associated with higher risk of all-cause mortality. A large number of studies evaluated MMPs pattern in obesity, diabetes mellitus, arterial hypertension and dyslipidemia, all of which define metabolic syndrome according to several Consensus Statement (i.e. IDF, ATP III, AHA). However, few research have been carried out on subjects with metabolic syndrome. The evidences of an improvement in MMP/TIMP ratio with diet, exercise and medical therapy should encourage further investigations with the intent to contrast the atherosclerotic process and to reduce morbidity and mortality of this kind of patients.