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Targeting vulnerable atherosclerotic plaque via PET-tracers aiming at cell-surface overexpression of somatostatin receptors
Cardiovascular disease (CD) is the leading cause of death in the developed world, with major atherothrombotic events, being mainly attributed to the rupture of unstable, vulnerable atherosclerotic lesions, leading to blood flow obstruction. Since unstable atherosclerotic plaques frequently do not ca...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7391298/ https://www.ncbi.nlm.nih.gov/pubmed/32765848 http://dx.doi.org/10.3892/br.2020.1316 |
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author | Z. Papadakis, Georgios Kochiadakis, George Lazopoulos, George Marias, Kostas Klapsinos, Nikolaos Hannah-Shmouni, Fady G. Igoumenaki, Georgia Konstantinos Nikolouzakis, Taxiarchis Kteniadakis, Stelios A. Spandidos, Demetrios H. Karantanas, Apostolos |
author_facet | Z. Papadakis, Georgios Kochiadakis, George Lazopoulos, George Marias, Kostas Klapsinos, Nikolaos Hannah-Shmouni, Fady G. Igoumenaki, Georgia Konstantinos Nikolouzakis, Taxiarchis Kteniadakis, Stelios A. Spandidos, Demetrios H. Karantanas, Apostolos |
author_sort | Z. Papadakis, Georgios |
collection | PubMed |
description | Cardiovascular disease (CD) is the leading cause of death in the developed world, with major atherothrombotic events, being mainly attributed to the rupture of unstable, vulnerable atherosclerotic lesions, leading to blood flow obstruction. Since unstable atherosclerotic plaques frequently do not cause hemodynamically significant blood flow restriction, conventional stress imaging tests cannot depict the vulnerable, high-risk for rupture atherosclerotic lesions. Therefore, molecular imaging techniques targeting specific pathophysiologic features related to atherosclerotic plaque rupture mechanism, hold promise for precise and individualized treatment strategies of CD. In the current report, we describe in a patient diagnosed with pancreatic neuroendocrine tumor, the selective uptake of (68)Ga-DOATATE by an atherosclerotic lesion in the thoracic aorta. This data indicates that (68)Ga-DOTATATE, which is a positron emitting tomography tracer, targeting the recruitment of macrophages taking place in the vulnerable plaque, could potentially serve as an imaging probe for the detection of high-risk, prone to rupture plaques. |
format | Online Article Text |
id | pubmed-7391298 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-73912982020-08-05 Targeting vulnerable atherosclerotic plaque via PET-tracers aiming at cell-surface overexpression of somatostatin receptors Z. Papadakis, Georgios Kochiadakis, George Lazopoulos, George Marias, Kostas Klapsinos, Nikolaos Hannah-Shmouni, Fady G. Igoumenaki, Georgia Konstantinos Nikolouzakis, Taxiarchis Kteniadakis, Stelios A. Spandidos, Demetrios H. Karantanas, Apostolos Biomed Rep Articles Cardiovascular disease (CD) is the leading cause of death in the developed world, with major atherothrombotic events, being mainly attributed to the rupture of unstable, vulnerable atherosclerotic lesions, leading to blood flow obstruction. Since unstable atherosclerotic plaques frequently do not cause hemodynamically significant blood flow restriction, conventional stress imaging tests cannot depict the vulnerable, high-risk for rupture atherosclerotic lesions. Therefore, molecular imaging techniques targeting specific pathophysiologic features related to atherosclerotic plaque rupture mechanism, hold promise for precise and individualized treatment strategies of CD. In the current report, we describe in a patient diagnosed with pancreatic neuroendocrine tumor, the selective uptake of (68)Ga-DOATATE by an atherosclerotic lesion in the thoracic aorta. This data indicates that (68)Ga-DOTATATE, which is a positron emitting tomography tracer, targeting the recruitment of macrophages taking place in the vulnerable plaque, could potentially serve as an imaging probe for the detection of high-risk, prone to rupture plaques. D.A. Spandidos 2020-09 2020-06-16 /pmc/articles/PMC7391298/ /pubmed/32765848 http://dx.doi.org/10.3892/br.2020.1316 Text en Copyright: © Z. Papadakis et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Z. Papadakis, Georgios Kochiadakis, George Lazopoulos, George Marias, Kostas Klapsinos, Nikolaos Hannah-Shmouni, Fady G. Igoumenaki, Georgia Konstantinos Nikolouzakis, Taxiarchis Kteniadakis, Stelios A. Spandidos, Demetrios H. Karantanas, Apostolos Targeting vulnerable atherosclerotic plaque via PET-tracers aiming at cell-surface overexpression of somatostatin receptors |
title | Targeting vulnerable atherosclerotic plaque via PET-tracers aiming at cell-surface overexpression of somatostatin receptors |
title_full | Targeting vulnerable atherosclerotic plaque via PET-tracers aiming at cell-surface overexpression of somatostatin receptors |
title_fullStr | Targeting vulnerable atherosclerotic plaque via PET-tracers aiming at cell-surface overexpression of somatostatin receptors |
title_full_unstemmed | Targeting vulnerable atherosclerotic plaque via PET-tracers aiming at cell-surface overexpression of somatostatin receptors |
title_short | Targeting vulnerable atherosclerotic plaque via PET-tracers aiming at cell-surface overexpression of somatostatin receptors |
title_sort | targeting vulnerable atherosclerotic plaque via pet-tracers aiming at cell-surface overexpression of somatostatin receptors |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7391298/ https://www.ncbi.nlm.nih.gov/pubmed/32765848 http://dx.doi.org/10.3892/br.2020.1316 |
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