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Role of Apoptosis in Amplifying Inflammatory Responses in Lung Diseases
Apoptosis is an important contributor to the pathophysiology of lung diseases such as acute lung injury (ALI) and chronic obstructive pulmonary disease (COPD). Furthermore, the cellular environment of these acute and chronic lung diseases favors the delayed clearance of apoptotic cells. This dysfunc...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3213897/ https://www.ncbi.nlm.nih.gov/pubmed/22081757 http://dx.doi.org/10.4137/JCD.S5375 |
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author | Schmidt, E.P. Tuder, R.M. |
author_facet | Schmidt, E.P. Tuder, R.M. |
author_sort | Schmidt, E.P. |
collection | PubMed |
description | Apoptosis is an important contributor to the pathophysiology of lung diseases such as acute lung injury (ALI) and chronic obstructive pulmonary disease (COPD). Furthermore, the cellular environment of these acute and chronic lung diseases favors the delayed clearance of apoptotic cells. This dysfunctional efferocytosis predisposes to the release of endogenous ligands from dying cells. These so-called damage-associated molecular patterns (DAMPs) play an important role in the stimulation of innate immunity as well as in the induction of adaptive immunity, potentially against autoantigens. In this review, we explore the role of apoptosis in ALI and COPD, with particular attention to the contribution of DAMP release in augmenting the inflammatory response in these disease states. |
format | Online Article Text |
id | pubmed-3213897 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-32138972011-11-11 Role of Apoptosis in Amplifying Inflammatory Responses in Lung Diseases Schmidt, E.P. Tuder, R.M. J Cell Death Review Apoptosis is an important contributor to the pathophysiology of lung diseases such as acute lung injury (ALI) and chronic obstructive pulmonary disease (COPD). Furthermore, the cellular environment of these acute and chronic lung diseases favors the delayed clearance of apoptotic cells. This dysfunctional efferocytosis predisposes to the release of endogenous ligands from dying cells. These so-called damage-associated molecular patterns (DAMPs) play an important role in the stimulation of innate immunity as well as in the induction of adaptive immunity, potentially against autoantigens. In this review, we explore the role of apoptosis in ALI and COPD, with particular attention to the contribution of DAMP release in augmenting the inflammatory response in these disease states. SAGE Publications 2010-07-22 /pmc/articles/PMC3213897/ /pubmed/22081757 http://dx.doi.org/10.4137/JCD.S5375 Text en © 2010 SAGE Publications. http://creativecommons.org/licenses/by-nc/3.0/ This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 3.0 License (http://www.creativecommons.org/licenses/by-nc/3.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access page (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Review Schmidt, E.P. Tuder, R.M. Role of Apoptosis in Amplifying Inflammatory Responses in Lung Diseases |
title | Role of Apoptosis in Amplifying Inflammatory Responses in Lung Diseases |
title_full | Role of Apoptosis in Amplifying Inflammatory Responses in Lung Diseases |
title_fullStr | Role of Apoptosis in Amplifying Inflammatory Responses in Lung Diseases |
title_full_unstemmed | Role of Apoptosis in Amplifying Inflammatory Responses in Lung Diseases |
title_short | Role of Apoptosis in Amplifying Inflammatory Responses in Lung Diseases |
title_sort | role of apoptosis in amplifying inflammatory responses in lung diseases |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3213897/ https://www.ncbi.nlm.nih.gov/pubmed/22081757 http://dx.doi.org/10.4137/JCD.S5375 |
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