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Open AccessReview

Molecular Imaging of Vulnerable Atherosclerotic Plaques in Animal Models

Institute of Biostructure and Bioimaging, National Research Council, Via T. De Amicis 95, 80145 Naples, Italy
Author to whom correspondence should be addressed.
Academic Editor: Michael Henein
Int. J. Mol. Sci. 2016, 17(9), 1511;
Received: 26 July 2016 / Revised: 24 August 2016 / Accepted: 31 August 2016 / Published: 9 September 2016
(This article belongs to the Special Issue Atherosclerosis and Vascular Imaging 2016)
Atherosclerosis is characterized by intimal plaques of the arterial vessels that develop slowly and, in some cases, may undergo spontaneous rupture with subsequent heart attack or stroke. Currently, noninvasive diagnostic tools are inadequate to screen atherosclerotic lesions at high risk of acute complications. Therefore, the attention of the scientific community has been focused on the use of molecular imaging for identifying vulnerable plaques. Genetically engineered murine models such as ApoE−/− and ApoE−/−Fbn1C1039G+/− mice have been shown to be useful for testing new probes targeting biomarkers of relevant molecular processes for the characterization of vulnerable plaques, such as vascular endothelial growth factor receptor (VEGFR)-1, VEGFR-2, intercellular adhesion molecule (ICAM)-1, P-selectin, and integrins, and for the potential development of translational tools to identify high-risk patients who could benefit from early therapeutic interventions. This review summarizes the main animal models of vulnerable plaques, with an emphasis on genetically altered mice, and the state-of-the-art preclinical molecular imaging strategies. View Full-Text
Keywords: atherosclerosis; vulnerable plaques; animal models; genetically modified mice; molecular imaging atherosclerosis; vulnerable plaques; animal models; genetically modified mice; molecular imaging
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MDPI and ACS Style

Gargiulo, S.; Gramanzini, M.; Mancini, M. Molecular Imaging of Vulnerable Atherosclerotic Plaques in Animal Models. Int. J. Mol. Sci. 2016, 17, 1511.

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