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Role of cytokines in myocardial ischemia and reperfusion
Mediators of myocardial inflammation, predominantly cytokines, have for many years been implicated in the healing processes after infarction. In recent years, however, more attention has been paid to the possibility that the inflammation may result in deleterious complications for myocardial infarct...
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Formato: | Texto |
Lenguaje: | English |
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Hindawi Publishing Corporation
1997
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365828/ https://www.ncbi.nlm.nih.gov/pubmed/18472818 http://dx.doi.org/10.1080/09629359791668 |
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author | Sharma, H. S. Das, D. K. |
author_facet | Sharma, H. S. Das, D. K. |
author_sort | Sharma, H. S. |
collection | PubMed |
description | Mediators of myocardial inflammation, predominantly cytokines, have for many years been implicated in the healing processes after infarction. In recent years, however, more attention has been paid to the possibility that the inflammation may result in deleterious complications for myocardial infarction. The proinflammatory cytokines may mediate myocardial dysfunction associated with myocardial infarction, severe congestive heart failure, and sepsis. A growing body of literature suggests that inflammatory mediators could play a crucial role in ischemia–reperfusion injury. Furthermore, ischemia–reperfusion not only results in the local transcriptional and translational upregulation of cytokines but also leads to tissue infiltration by inflammatory cells. These inflammatory cells are a ready source of a variety of cytokines which could be lethal for the cardiomyocytes. At the cellular level it has been shown that hypoxia causes a series of well documented changes in cardiomyocytes that includes loss of contractility, changes in lipid metabolism and subsequent irreversible cell membrane damage leading to cell death. For instance, hypoxic cardiomyocytes produce interleukin-6 (IL-6) which could contribute to the myocardial dysfunction observed in ischemia reperfusion injury. Ischemia followed by reperfusion induces a number of other multi-potent cytokines, such as IL-1, IL-8, tumor necrosis factor-α (TNF-α), transforming growth factor-β1 (TGF-β1) as well as an angiogenic cytokine/ growth factor, vascular endothelial growth factor (VEGF), in the heart. Intrestingly, these multipotent cytokines (e.g. TNF-α) may induce an adaptive cytoprotective response in the reperfused myocardium. In this review, we have included a number of cytokines that may contribute to ventricular dysfunction and/or to the cytoprotective and adaptive changes in the reperfused heart. |
format | Text |
id | pubmed-2365828 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 1997 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-23658282008-05-12 Role of cytokines in myocardial ischemia and reperfusion Sharma, H. S. Das, D. K. Mediators Inflamm Research Article Mediators of myocardial inflammation, predominantly cytokines, have for many years been implicated in the healing processes after infarction. In recent years, however, more attention has been paid to the possibility that the inflammation may result in deleterious complications for myocardial infarction. The proinflammatory cytokines may mediate myocardial dysfunction associated with myocardial infarction, severe congestive heart failure, and sepsis. A growing body of literature suggests that inflammatory mediators could play a crucial role in ischemia–reperfusion injury. Furthermore, ischemia–reperfusion not only results in the local transcriptional and translational upregulation of cytokines but also leads to tissue infiltration by inflammatory cells. These inflammatory cells are a ready source of a variety of cytokines which could be lethal for the cardiomyocytes. At the cellular level it has been shown that hypoxia causes a series of well documented changes in cardiomyocytes that includes loss of contractility, changes in lipid metabolism and subsequent irreversible cell membrane damage leading to cell death. For instance, hypoxic cardiomyocytes produce interleukin-6 (IL-6) which could contribute to the myocardial dysfunction observed in ischemia reperfusion injury. Ischemia followed by reperfusion induces a number of other multi-potent cytokines, such as IL-1, IL-8, tumor necrosis factor-α (TNF-α), transforming growth factor-β1 (TGF-β1) as well as an angiogenic cytokine/ growth factor, vascular endothelial growth factor (VEGF), in the heart. Intrestingly, these multipotent cytokines (e.g. TNF-α) may induce an adaptive cytoprotective response in the reperfused myocardium. In this review, we have included a number of cytokines that may contribute to ventricular dysfunction and/or to the cytoprotective and adaptive changes in the reperfused heart. Hindawi Publishing Corporation 1997-06 /pmc/articles/PMC2365828/ /pubmed/18472818 http://dx.doi.org/10.1080/09629359791668 Text en Copyright © 1997 Hindawi Publishing Corporation. http://creativecommons.org/licenses/by/ 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 | Research Article Sharma, H. S. Das, D. K. Role of cytokines in myocardial ischemia and reperfusion |
title | Role of cytokines in myocardial ischemia and reperfusion |
title_full | Role of cytokines in myocardial ischemia and reperfusion |
title_fullStr | Role of cytokines in myocardial ischemia and reperfusion |
title_full_unstemmed | Role of cytokines in myocardial ischemia and reperfusion |
title_short | Role of cytokines in myocardial ischemia and reperfusion |
title_sort | role of cytokines in myocardial ischemia and reperfusion |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2365828/ https://www.ncbi.nlm.nih.gov/pubmed/18472818 http://dx.doi.org/10.1080/09629359791668 |
work_keys_str_mv | AT sharmahs roleofcytokinesinmyocardialischemiaandreperfusion AT dasdk roleofcytokinesinmyocardialischemiaandreperfusion |