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Mediators of Inflammation
Volume 2013 (2013), Article ID 725102, 10 pages
http://dx.doi.org/10.1155/2013/725102
Review Article

Long Pentraxin 3: Experimental and Clinical Relevance in Cardiovascular Diseases

1Department of Pharmacological and Biomolecular Sciences, Università Degli Studi di Milano, 20133 Milan, Italy
2Center for the Study of Atherosclerosis, Ospedale Bassini, 20092 Cinisello Balsamo, Italy
3IRCCS Multimedica, 20162 Milan, Italy
4The Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University, London E1 2AT, UK

Received 21 December 2012; Accepted 27 February 2013

Academic Editor: Austin Meng Guo

Copyright © 2013 Fabrizia Bonacina 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.

Abstract

Pentraxin 3 (PTX3) is an essential component of the humoral arm of innate immunity and belongs, together with the C-reactive protein (CRP) and other acute phase proteins, to the pentraxins' superfamily: soluble, multifunctional, pattern recognition proteins. Pentraxins share a common C-terminal pentraxin domain, which in the case of PTX3 is coupled to an unrelated long N-terminal domain. PTX3 in humans, like CRP, correlates with surrogate markers of atherosclerosis and is independently associated with the risk of developing vascular events. Studies addressing the potential physiopathological role of CRP in the cardiovascular system were so far inconclusive and have been limited by the fact that the sequence and regulation have not been conserved during evolution between mouse and man. On the contrary, the conservation of sequence, gene organization, and regulation of PTX3 supports the translation of animal model findings in humans. While PTX3 deficiency is associated with increased inflammation, cardiac damage, and atherosclerosis, the overexpression limits carotid restenosis after angioplasty. These observations point to a cardiovascular protective effect of PTX3 potentially associated with the ability of tuning inflammation and favor the hypothesis that the increased levels of PTX3 in subjects with cardiovascular diseases may reflect a protective physiological mechanism, which correlates with the immunoinflammatory response observed in several cardiovascular disorders.