Background Diabetes mellitus (DM) and chronic inflammation are strongly related to increased cardiovascular risk. The purpose of this study was to evaluate whet...

SUMMARYBackground: Aortic abdominal aneurysm (AAA) represents a common chronic degenerative disease of the aortic wall. Chronic inflammation and enzymatic degradation of elastic lamellae and extracellular matrix (ECM) proteins constitute the most prominent characteristics of AAAs. There is mounting evidence that matrix metalloproteinases (MMPs) are the predominant proteinases in the AAA wall. These enzymes represent a potential target for therapeutic intervention to modify vascular pathology. This paper is an overview of matrix metalloproteinases and their role in the pathophysiology, diagnosis and treatment of AAA.Literature search: Comprehensive search of the MEDLINE, EMBASE and HEAL-Link databases from 1980 to 2003.Findings: Increased levels of MMPs expression and activity have been demonstrated within the aortic wall of AAA, associating with histological alterations. An imbalance between MMPs and their inhibitors (Tissue Inhibitors of Matrix Metalloproteinases – TIMPs), may tip the equilibrium towards...

Diabetes mellitus (DM) is associated with an increased incidence of cardiovascular events and microvascular complications. These complications contribute to the morbidity and mortality associated with DM. There is increasing evidence supporting a role for matrix metalloproteinases (MMPs) and their inhibitors (tissue inhibitors of matrix metalloproteinases—TIMPs) in the atherosclerotic process. However, the relationship between MMPs/TIMPs and diabetic angiopathy is less well defined. Hyperglycemia directly or indirectly (eg, via oxidative stress or advanced glycation products) increases MMP expression and activity. These changes are associated with histologic alterations in large vessels. On the other hand, low proteolytic activity of MMPs contributes to diabetic nephropathy. Within atherosclerotic plaques an imbalance between MMPs and TIMPs may induce matrix degradation, resulting in an increased risk of plaque rupture. Furthermore, because MMPs enhance blood coagulability, MMPs and TIMPs may play a role in acute thrombotic occlusion of vessels and consequent cardiovascular events. Some drugs can inhibit MMP activity. However, the precise mechanisms involved are still not defined. Further research is required to demonstrate the causative relationship between MMPs/TIMPs and diabetic atherosclerosis. It also remains to be established if the long-term administration of MMP inhibitors can prevent acute cardiovascular events.