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BioMed Research International
Volume 2013, Article ID 650989, 9 pages
Review Article

Lipoprotein(a) in Cardiovascular Diseases

1International Ph. D. Program in Neuropharmacology, University of Catania, 95123 Catania, Italy
2Department of Senescence, Urological, and Neurological Sciences, University of Catania, 95126 Catania, Italy
3Department of Biomedical Sciences, University of Catania, 95124 Catania, Italy
4Department of Neurosciences, University of Catania, 95123 Catania, Italy
5Department of Biological Chemistry, Medical Chemistry, and Molecular Biology, University of Catania, 95123 Catania, Italy
6Pediatric Cardiology and Cardiac Surgery Department, Guch Unit, IRCCS Policlinico San Donato, 20097 Milan, Italy

Received 6 September 2012; Revised 6 November 2012; Accepted 8 November 2012

Academic Editor: Joseph Fomusi Ndisang

Copyright © 2013 Michele Malaguarnera et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Lipoprotein(a) (Lp(a)) is an LDL-like molecule consisting of an apolipoprotein B-100 (apo(B-100)) particle attached by a disulphide bridge to apo(a). Many observations have pointed out that Lp(a) levels may be a risk factor for cardiovascular diseases. Lp(a) inhibits the activation of transforming growth factor (TGF) and contributes to the growth of arterial atherosclerotic lesions by promoting the proliferation of vascular smooth muscle cells and the migration of smooth muscle cells to endothelial cells. Moreover Lp(a) inhibits plasminogen binding to the surfaces of endothelial cells and decreases the activity of fibrin-dependent tissue-type plasminogen activator. Lp(a) may act as a proinflammatory mediator that augments the lesion formation in atherosclerotic plaques. Elevated serum Lp(a) is an independent predictor of coronary artery disease and myocardial infarction. Furthermore, Lp(a) levels should be a marker of restenosis after percutaneous transluminal coronary angioplasty, saphenous vein bypass graft atherosclerosis, and accelerated coronary atherosclerosis of cardiac transplantation. Finally, the possibility that Lp(a) may be a risk factor for ischemic stroke has been assessed in several studies. Recent findings suggest that Lp(a)-lowering therapy might be beneficial in patients with high Lp(a) levels. A future therapeutic approach could include apheresis in high-risk patients in order to reduce major coronary events.