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Statins as a novel therapeutic strategy in acute lung injury

Acute lung injury (ALI) is a devastating clinical condition associated with pulmonary and systemic inflammation and characterized by incompetence of the pulmonary microvascular barrier culminating in noncardiogenic pulmonary edema. An understanding of the mechanisms underlying endothelial barrier dy...

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Detalles Bibliográficos
Autores principales: Singla, Sunit, Jacobson, Jeffrey R.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Medknow Publications & Media Pvt Ltd 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3555410/
https://www.ncbi.nlm.nih.gov/pubmed/23372924
http://dx.doi.org/10.4103/2045-8932.105028
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author Singla, Sunit
Jacobson, Jeffrey R.
author_facet Singla, Sunit
Jacobson, Jeffrey R.
author_sort Singla, Sunit
collection PubMed
description Acute lung injury (ALI) is a devastating clinical condition associated with pulmonary and systemic inflammation and characterized by incompetence of the pulmonary microvascular barrier culminating in noncardiogenic pulmonary edema. An understanding of the mechanisms underlying endothelial barrier dysfunction in ALI has been facilitated by study of the effects of statins in relevant cellular and animals models. Many of the pleotropic properties of these drugs, including direct effects on endothelial cell (EC) cytoskeletal rearrangement, NADPH oxidase, and nitric oxide activity, as well as effects on differential EC gene expression, are relevant to the pathobiology of ALI and suggest a potential therapeutic role for statins in this context. Moreover, results from preclinical studies and observations in relevant patient populations support the protective potential of statins in ALI, paving the way now for definitive clinical trials.
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spelling pubmed-35554102013-01-31 Statins as a novel therapeutic strategy in acute lung injury Singla, Sunit Jacobson, Jeffrey R. Pulm Circ Review Article Acute lung injury (ALI) is a devastating clinical condition associated with pulmonary and systemic inflammation and characterized by incompetence of the pulmonary microvascular barrier culminating in noncardiogenic pulmonary edema. An understanding of the mechanisms underlying endothelial barrier dysfunction in ALI has been facilitated by study of the effects of statins in relevant cellular and animals models. Many of the pleotropic properties of these drugs, including direct effects on endothelial cell (EC) cytoskeletal rearrangement, NADPH oxidase, and nitric oxide activity, as well as effects on differential EC gene expression, are relevant to the pathobiology of ALI and suggest a potential therapeutic role for statins in this context. Moreover, results from preclinical studies and observations in relevant patient populations support the protective potential of statins in ALI, paving the way now for definitive clinical trials. Medknow Publications & Media Pvt Ltd 2012 /pmc/articles/PMC3555410/ /pubmed/23372924 http://dx.doi.org/10.4103/2045-8932.105028 Text en Copyright: © Pulmonary Circulation http://creativecommons.org/licenses/by-nc-sa/3.0 This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Singla, Sunit
Jacobson, Jeffrey R.
Statins as a novel therapeutic strategy in acute lung injury
title Statins as a novel therapeutic strategy in acute lung injury
title_full Statins as a novel therapeutic strategy in acute lung injury
title_fullStr Statins as a novel therapeutic strategy in acute lung injury
title_full_unstemmed Statins as a novel therapeutic strategy in acute lung injury
title_short Statins as a novel therapeutic strategy in acute lung injury
title_sort statins as a novel therapeutic strategy in acute lung injury
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3555410/
https://www.ncbi.nlm.nih.gov/pubmed/23372924
http://dx.doi.org/10.4103/2045-8932.105028
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