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Post-infarct remodelling: contribution of wound healing and inflammation
In human and experimental myocardial infarction (MI), cessation of blood supply leads to rapid necrosis of cardiac myocytes in the ischaemic heart. Immediately after injury, various intra- and intercellular pathways contribute to healing the myocardial wound in order to achieve tissue integrity and...
Autores principales: | , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
Oxford University Press
2009
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2639128/ https://www.ncbi.nlm.nih.gov/pubmed/18977766 http://dx.doi.org/10.1093/cvr/cvn292 |
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author | Frantz, Stefan Bauersachs, Johann Ertl, Georg |
author_facet | Frantz, Stefan Bauersachs, Johann Ertl, Georg |
author_sort | Frantz, Stefan |
collection | PubMed |
description | In human and experimental myocardial infarction (MI), cessation of blood supply leads to rapid necrosis of cardiac myocytes in the ischaemic heart. Immediately after injury, various intra- and intercellular pathways contribute to healing the myocardial wound in order to achieve tissue integrity and function. MI and the consequent loss of myocardium are the major aetiology for heart failure. Despite aggressive primary therapy, prognosis remains poor in patients with large infarction and severe left ventricular dysfunction. Thus, it would be highly desirable to improve healing of the cardiac wound to maintain structure and function of the heart. Healing in the heart occurs in overlapping phases. Herein, we review the inflammatory phase as a trigger of tissue formation. |
format | Text |
id | pubmed-2639128 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2009 |
publisher | Oxford University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-26391282009-02-25 Post-infarct remodelling: contribution of wound healing and inflammation Frantz, Stefan Bauersachs, Johann Ertl, Georg Cardiovasc Res Reviews In human and experimental myocardial infarction (MI), cessation of blood supply leads to rapid necrosis of cardiac myocytes in the ischaemic heart. Immediately after injury, various intra- and intercellular pathways contribute to healing the myocardial wound in order to achieve tissue integrity and function. MI and the consequent loss of myocardium are the major aetiology for heart failure. Despite aggressive primary therapy, prognosis remains poor in patients with large infarction and severe left ventricular dysfunction. Thus, it would be highly desirable to improve healing of the cardiac wound to maintain structure and function of the heart. Healing in the heart occurs in overlapping phases. Herein, we review the inflammatory phase as a trigger of tissue formation. Oxford University Press 2009-02-15 2008-10-31 /pmc/articles/PMC2639128/ /pubmed/18977766 http://dx.doi.org/10.1093/cvr/cvn292 Text en Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org |
spellingShingle | Reviews Frantz, Stefan Bauersachs, Johann Ertl, Georg Post-infarct remodelling: contribution of wound healing and inflammation |
title | Post-infarct remodelling: contribution of wound healing and inflammation |
title_full | Post-infarct remodelling: contribution of wound healing and inflammation |
title_fullStr | Post-infarct remodelling: contribution of wound healing and inflammation |
title_full_unstemmed | Post-infarct remodelling: contribution of wound healing and inflammation |
title_short | Post-infarct remodelling: contribution of wound healing and inflammation |
title_sort | post-infarct remodelling: contribution of wound healing and inflammation |
topic | Reviews |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2639128/ https://www.ncbi.nlm.nih.gov/pubmed/18977766 http://dx.doi.org/10.1093/cvr/cvn292 |
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