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Administration of synthetic MMP inhibitors in experimental animal models of these cardiovascular diseases significantly inhibits the progression of, respectively, atherosclerotic lesion formation, neointima formation, left ventricular remodeling, pump dysfunction, and infarct healing. This review focuses on the role of MMPs in cardiovascular disease, in particular myocardial infarction and the subsequent progression to heart failure. MMPs, which are present in the myocardium and capable of degrading all the matrix components of the heart, are the driving force behind myocardial matrix remodeling. The recent finding that acute pharmacological inhibition of MMPs or deficiency in MMP-9 attenuates left ventricular dilatation in the infarcted mouse heart led to the proposal that MMP inhibitors could be used as a potential therapy for patients at risk for the development of heart failure after myocardial infarction. Although these promising results encourage the design of clinical trials with MMP inhibitors, there are still several unresolved issues. This review describes the biology of MMPs and discusses new insights into the role of MMPs in several cardiovascular diseases. Attention will be paid to the central role of the plasminogen system as an important activator of MMPs in the remodeling process after myocardial infarction. Finally, we speculate on the use of MMP inhibitors as potential therapy for heart failure.<\/jats:p>","DOI":"10.1161\/hh1501.094396","type":"journal-article","created":{"date-parts":[[2007,9,28]],"date-time":"2007-09-28T14:32:49Z","timestamp":1190989969000},"page":"201-210","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":460,"title":["Matrix Metalloproteinase Inhibition After Myocardial Infarction"],"prefix":"10.1161","volume":"89","author":[{"given":"Esther E.J.M.","family":"Creemers","sequence":"first","affiliation":[{"name":"From the Departments of Pathology (E.E.J.M.C., J.P.M.C., M.J.A.P.D.) and Pharmacology (J.F.M.S.), Cardiovascular Research Institute Maastricht, University of Maastricht, The Netherlands."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jack P.M.","family":"Cleutjens","sequence":"additional","affiliation":[{"name":"From the Departments of Pathology (E.E.J.M.C., J.P.M.C., M.J.A.P.D.) and Pharmacology (J.F.M.S.), Cardiovascular Research Institute Maastricht, University of Maastricht, The Netherlands."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jos F.M.","family":"Smits","sequence":"additional","affiliation":[{"name":"From the Departments of Pathology (E.E.J.M.C., J.P.M.C., M.J.A.P.D.) and Pharmacology (J.F.M.S.), Cardiovascular Research Institute Maastricht, University of Maastricht, The Netherlands."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mat J.A.P.","family":"Daemen","sequence":"additional","affiliation":[{"name":"From the Departments of Pathology (E.E.J.M.C., J.P.M.C., M.J.A.P.D.) and Pharmacology (J.F.M.S.), Cardiovascular Research Institute Maastricht, University of Maastricht, The Netherlands."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_3_1_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.78.1.2968197"},{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.81.4.2138525"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1139\/y92-130"},{"key":"e_1_3_3_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.84.5.1934383"},{"key":"e_1_3_3_5_2","doi-asserted-by":"publisher","DOI":"10.1172\/JCI8040"},{"key":"e_1_3_3_6_2","first-page":"311","volume":"72","year":"1995","unstructured":"Okada Y, Nara K, Kawamura K. 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