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Endoplasmic Reticulum Stress and the Related Signaling Networks in Severe Asthma

The endoplasmic reticulum (ER) is a specialized organelle that plays a central role in biosynthesis, correct protein folding, and posttranslational modifications of secretory and membrane proteins. Loss of homeostasis in ER functions triggers the ER stress response, resulting in activation of unfold...

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Detalles Bibliográficos
Autores principales: Kim, So Ri, Lee, Yong Chul
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Academy of Asthma, Allergy and Clinical Immunology; The Korean Academy of Pediatric Allergy and Respiratory Disease 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4341331/
https://www.ncbi.nlm.nih.gov/pubmed/25729617
http://dx.doi.org/10.4168/aair.2015.7.2.106
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author Kim, So Ri
Lee, Yong Chul
author_facet Kim, So Ri
Lee, Yong Chul
author_sort Kim, So Ri
collection PubMed
description The endoplasmic reticulum (ER) is a specialized organelle that plays a central role in biosynthesis, correct protein folding, and posttranslational modifications of secretory and membrane proteins. Loss of homeostasis in ER functions triggers the ER stress response, resulting in activation of unfolded protein response (UPR), a hallmark of many inflammatory diseases. These pathways have been reported as critical players in the pathogenesis of various pulmonary disorders, including pulmonary fibrosis, lung injury, and chronic airway disorders. More interestingly, ER stress and the related signaling networks are emerging as important modulators of inflammatory and immune responses in the development of allergen-induced bronchial asthma, especially severe asthma.
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spelling pubmed-43413312015-03-01 Endoplasmic Reticulum Stress and the Related Signaling Networks in Severe Asthma Kim, So Ri Lee, Yong Chul Allergy Asthma Immunol Res Review The endoplasmic reticulum (ER) is a specialized organelle that plays a central role in biosynthesis, correct protein folding, and posttranslational modifications of secretory and membrane proteins. Loss of homeostasis in ER functions triggers the ER stress response, resulting in activation of unfolded protein response (UPR), a hallmark of many inflammatory diseases. These pathways have been reported as critical players in the pathogenesis of various pulmonary disorders, including pulmonary fibrosis, lung injury, and chronic airway disorders. More interestingly, ER stress and the related signaling networks are emerging as important modulators of inflammatory and immune responses in the development of allergen-induced bronchial asthma, especially severe asthma. The Korean Academy of Asthma, Allergy and Clinical Immunology; The Korean Academy of Pediatric Allergy and Respiratory Disease 2015-03 2014-10-17 /pmc/articles/PMC4341331/ /pubmed/25729617 http://dx.doi.org/10.4168/aair.2015.7.2.106 Text en Copyright © 2015 The Korean Academy of Asthma, Allergy and Clinical Immunology • The Korean Academy of Pediatric Allergy and Respiratory Disease http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review
Kim, So Ri
Lee, Yong Chul
Endoplasmic Reticulum Stress and the Related Signaling Networks in Severe Asthma
title Endoplasmic Reticulum Stress and the Related Signaling Networks in Severe Asthma
title_full Endoplasmic Reticulum Stress and the Related Signaling Networks in Severe Asthma
title_fullStr Endoplasmic Reticulum Stress and the Related Signaling Networks in Severe Asthma
title_full_unstemmed Endoplasmic Reticulum Stress and the Related Signaling Networks in Severe Asthma
title_short Endoplasmic Reticulum Stress and the Related Signaling Networks in Severe Asthma
title_sort endoplasmic reticulum stress and the related signaling networks in severe asthma
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4341331/
https://www.ncbi.nlm.nih.gov/pubmed/25729617
http://dx.doi.org/10.4168/aair.2015.7.2.106
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