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Endoplasmic Reticulum Stress-Related Inflammation and Cardiovascular Diseases

The endoplasmic reticulum (ER) is the site of synthesis and maturation of proteins designed for secretion or for localization on the cell membrane. Various types of stress from both inside and outside cells disturb ER function, thus causing unfolded or misfolded proteins to accumulate in the ER. To...

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Detalles Bibliográficos
Autores principales: Gotoh, Tomomi, Endo, Motoyoshi, Oike, Yuichi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE-Hindawi Access to Research 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3132612/
https://www.ncbi.nlm.nih.gov/pubmed/21755026
http://dx.doi.org/10.4061/2011/259462
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author Gotoh, Tomomi
Endo, Motoyoshi
Oike, Yuichi
author_facet Gotoh, Tomomi
Endo, Motoyoshi
Oike, Yuichi
author_sort Gotoh, Tomomi
collection PubMed
description The endoplasmic reticulum (ER) is the site of synthesis and maturation of proteins designed for secretion or for localization on the cell membrane. Various types of stress from both inside and outside cells disturb ER function, thus causing unfolded or misfolded proteins to accumulate in the ER. To improve and maintain the ER functions against such stresses, the ER stress response pathway is activated. However, when the stress is prolonged or severe, apoptosis pathways are activated to remove damaged cells. It was recently reported that the ER stress pathway is also involved in the inflammatory response, whereby inflammation induces ER stress, and ER stress induces an inflammatory response. Therefore, the ER stress response pathway is involved in various diseases, including cardiovascular diseases such as atherosclerosis and ischemic diseases, in various ways. The ER stress pathway may represent a novel target for the treatment of these diseases.
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spelling pubmed-31326122011-07-13 Endoplasmic Reticulum Stress-Related Inflammation and Cardiovascular Diseases Gotoh, Tomomi Endo, Motoyoshi Oike, Yuichi Int J Inflam Review Article The endoplasmic reticulum (ER) is the site of synthesis and maturation of proteins designed for secretion or for localization on the cell membrane. Various types of stress from both inside and outside cells disturb ER function, thus causing unfolded or misfolded proteins to accumulate in the ER. To improve and maintain the ER functions against such stresses, the ER stress response pathway is activated. However, when the stress is prolonged or severe, apoptosis pathways are activated to remove damaged cells. It was recently reported that the ER stress pathway is also involved in the inflammatory response, whereby inflammation induces ER stress, and ER stress induces an inflammatory response. Therefore, the ER stress response pathway is involved in various diseases, including cardiovascular diseases such as atherosclerosis and ischemic diseases, in various ways. The ER stress pathway may represent a novel target for the treatment of these diseases. SAGE-Hindawi Access to Research 2011-06-27 /pmc/articles/PMC3132612/ /pubmed/21755026 http://dx.doi.org/10.4061/2011/259462 Text en Copyright © 2011 Tomomi Gotoh et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Gotoh, Tomomi
Endo, Motoyoshi
Oike, Yuichi
Endoplasmic Reticulum Stress-Related Inflammation and Cardiovascular Diseases
title Endoplasmic Reticulum Stress-Related Inflammation and Cardiovascular Diseases
title_full Endoplasmic Reticulum Stress-Related Inflammation and Cardiovascular Diseases
title_fullStr Endoplasmic Reticulum Stress-Related Inflammation and Cardiovascular Diseases
title_full_unstemmed Endoplasmic Reticulum Stress-Related Inflammation and Cardiovascular Diseases
title_short Endoplasmic Reticulum Stress-Related Inflammation and Cardiovascular Diseases
title_sort endoplasmic reticulum stress-related inflammation and cardiovascular diseases
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3132612/
https://www.ncbi.nlm.nih.gov/pubmed/21755026
http://dx.doi.org/10.4061/2011/259462
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