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Autophagy facilitates ventilator-induced lung injury partly through activation of NF-κB pathway

Mechanical ventilation is an important supportive therapy in the intensive care unit (ICU) to assist the critically ill patients with respiratory failure. But longer ventilation time has been proven to contribute to the lung injury which has been recognized as ventilator-induced lung injury (VILI)....

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Autores principales: Gao, Min, Liu, Donglei, Du, Yuming, Sun, Rongqing, Zhao, Luosha
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3871487/
https://www.ncbi.nlm.nih.gov/pubmed/24343346
http://dx.doi.org/10.12659/MSM.889746
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author Gao, Min
Liu, Donglei
Du, Yuming
Sun, Rongqing
Zhao, Luosha
author_facet Gao, Min
Liu, Donglei
Du, Yuming
Sun, Rongqing
Zhao, Luosha
author_sort Gao, Min
collection PubMed
description Mechanical ventilation is an important supportive therapy in the intensive care unit (ICU) to assist the critically ill patients with respiratory failure. But longer ventilation time has been proven to contribute to the lung injury which has been recognized as ventilator-induced lung injury (VILI). Recently studies have suggested that NF-κB signaling pathways may play a critical role in the process of inflammation and autophagy, and autophagy can reduce the damage of VILI partly by activating the NF-κB pathways. Thus, we propose that autophagy may facilitate ventilator-induced lung injury partly through activation of NF-κB pathway, which might be a new potential therapeutic target for ventilator-induced lung injury. Although the exact mechanism of autophagy and its exact role in the VILI need to be further explored, at least it provides us a potential target in the future prevention of VILI.
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spelling pubmed-38714872013-12-26 Autophagy facilitates ventilator-induced lung injury partly through activation of NF-κB pathway Gao, Min Liu, Donglei Du, Yuming Sun, Rongqing Zhao, Luosha Med Sci Monit Hypothesis Mechanical ventilation is an important supportive therapy in the intensive care unit (ICU) to assist the critically ill patients with respiratory failure. But longer ventilation time has been proven to contribute to the lung injury which has been recognized as ventilator-induced lung injury (VILI). Recently studies have suggested that NF-κB signaling pathways may play a critical role in the process of inflammation and autophagy, and autophagy can reduce the damage of VILI partly by activating the NF-κB pathways. Thus, we propose that autophagy may facilitate ventilator-induced lung injury partly through activation of NF-κB pathway, which might be a new potential therapeutic target for ventilator-induced lung injury. Although the exact mechanism of autophagy and its exact role in the VILI need to be further explored, at least it provides us a potential target in the future prevention of VILI. International Scientific Literature, Inc. 2013-12-17 /pmc/articles/PMC3871487/ /pubmed/24343346 http://dx.doi.org/10.12659/MSM.889746 Text en © Med Sci Monit, 2013 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License
spellingShingle Hypothesis
Gao, Min
Liu, Donglei
Du, Yuming
Sun, Rongqing
Zhao, Luosha
Autophagy facilitates ventilator-induced lung injury partly through activation of NF-κB pathway
title Autophagy facilitates ventilator-induced lung injury partly through activation of NF-κB pathway
title_full Autophagy facilitates ventilator-induced lung injury partly through activation of NF-κB pathway
title_fullStr Autophagy facilitates ventilator-induced lung injury partly through activation of NF-κB pathway
title_full_unstemmed Autophagy facilitates ventilator-induced lung injury partly through activation of NF-κB pathway
title_short Autophagy facilitates ventilator-induced lung injury partly through activation of NF-κB pathway
title_sort autophagy facilitates ventilator-induced lung injury partly through activation of nf-κb pathway
topic Hypothesis
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3871487/
https://www.ncbi.nlm.nih.gov/pubmed/24343346
http://dx.doi.org/10.12659/MSM.889746
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