Nikolaos Papageorgiou, Dimitris Tousoulis, George Hatzis, Alexandros Briasoulis, Emmanuel Androulakis, Anastasios Giolis, Gerasimos Siasos, George Latsios, Georgia Vogiatzi, Costas Tentolouris and Christodoulos Stefanadis Pages 1206 - 1213 ( 8 )
It is well established that matrix metalloproteinases (MMPs) contribute to the degradation of the extracellular matrix of coronary plaque and contribute to the thinning of the fibrous cap. As a result, the atheromatous plaque becomes unstable and prone to rupture with consequent clinical manifestations including acute coronary syndromes. Moreover, genetic polymorphisms of MMPs have been found to be associated with the concentration of circulating MMPs, and over the past decade, considerable efforts have been devoted to explore the relationships between MMPs polymorphisms and myocardial infarction risk among various populations. However, existing studies have yielded inconsistent results. Some observations have suggested that genetic variation that affects the expression of MMPs may contribute to the occurrence of myocardial infarction, whereas others reported no support for an association of MMPs polymorphisms with myocardial infarction susceptibility. Furthermore, the interpretation of these studies has been complicated by the use of different populations or different control sources. Therefore, further studies are required to evaluate the role of matrix metalloproteinases and especially the associated genetic polymorphisms in cardiovascular disease.
Matrix metalloproteinases, gene polymorphisms, atherosclerosis, coronary plaque, coronary artery disease, fibrous cap, acute coronary syndromes, myocardial infarction risk, matrix metalloproteinases, genetic polymorphisms, cardiovascular disease, occlusive thrombus, biologic pathway, risk factors
1st Cardiology Department, Hippokration Hospital, Athens University Medical School, Athens, Greece.