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Leukocyte Trafficking in Cardiovascular Disease: Insights from Experimental Models
Chemokine-induced leukocyte migration into the vessel wall is an early pathological event in the progression of atherosclerosis, the underlying cause of myocardial infarction. The immune-inflammatory response, mediated by both the innate and adaptive immune cells, is involved in the initiation, recr...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5390637/ https://www.ncbi.nlm.nih.gov/pubmed/28465628 http://dx.doi.org/10.1155/2017/9746169 |
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author | Jones, Daniel P. True, Harry D. Patel, Jyoti |
author_facet | Jones, Daniel P. True, Harry D. Patel, Jyoti |
author_sort | Jones, Daniel P. |
collection | PubMed |
description | Chemokine-induced leukocyte migration into the vessel wall is an early pathological event in the progression of atherosclerosis, the underlying cause of myocardial infarction. The immune-inflammatory response, mediated by both the innate and adaptive immune cells, is involved in the initiation, recruitment, and resolution phases of cardiovascular disease progression. Activation of leukocytes via inflammatory mediators such as chemokines, cytokines, and adhesion molecules is instrumental in these processes. In this review, we highlight leukocyte activation with the main focus being on the mechanisms of chemokine-mediated recruitment in atherosclerosis and the response postmyocardial infarction with key examples from experimental models of cardiovascular inflammation. |
format | Online Article Text |
id | pubmed-5390637 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Hindawi |
record_format | MEDLINE/PubMed |
spelling | pubmed-53906372017-05-02 Leukocyte Trafficking in Cardiovascular Disease: Insights from Experimental Models Jones, Daniel P. True, Harry D. Patel, Jyoti Mediators Inflamm Review Article Chemokine-induced leukocyte migration into the vessel wall is an early pathological event in the progression of atherosclerosis, the underlying cause of myocardial infarction. The immune-inflammatory response, mediated by both the innate and adaptive immune cells, is involved in the initiation, recruitment, and resolution phases of cardiovascular disease progression. Activation of leukocytes via inflammatory mediators such as chemokines, cytokines, and adhesion molecules is instrumental in these processes. In this review, we highlight leukocyte activation with the main focus being on the mechanisms of chemokine-mediated recruitment in atherosclerosis and the response postmyocardial infarction with key examples from experimental models of cardiovascular inflammation. Hindawi 2017 2017-03-30 /pmc/articles/PMC5390637/ /pubmed/28465628 http://dx.doi.org/10.1155/2017/9746169 Text en Copyright © 2017 Daniel P. Jones et al. http://creativecommons.org/licenses/by/4.0/ 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. |
spellingShingle | Review Article Jones, Daniel P. True, Harry D. Patel, Jyoti Leukocyte Trafficking in Cardiovascular Disease: Insights from Experimental Models |
title | Leukocyte Trafficking in Cardiovascular Disease: Insights from Experimental Models |
title_full | Leukocyte Trafficking in Cardiovascular Disease: Insights from Experimental Models |
title_fullStr | Leukocyte Trafficking in Cardiovascular Disease: Insights from Experimental Models |
title_full_unstemmed | Leukocyte Trafficking in Cardiovascular Disease: Insights from Experimental Models |
title_short | Leukocyte Trafficking in Cardiovascular Disease: Insights from Experimental Models |
title_sort | leukocyte trafficking in cardiovascular disease: insights from experimental models |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5390637/ https://www.ncbi.nlm.nih.gov/pubmed/28465628 http://dx.doi.org/10.1155/2017/9746169 |
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