Diabetes as a disease of endoplasmic reticulum stress

Endoplasmic reticulum (ER) stress is an integral part of life for all professional secretory cells, but it has been studied to greatest depth in the pancreatic β‐cell. This reflects both the crucial role played by ER stress in the pathogenesis of diabetes and also the exquisite vulnerability of thes...

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Published inDiabetes/metabolism research and reviews Vol. 26; no. 8; pp. 611 - 621
Main Authors Thomas, Sally E., Dalton, Lucy E., Daly, Marie-Louise, Malzer, Elke, Marciniak, Stefan J.
Format Journal Article
LanguageEnglish
Published Chichester, UK John Wiley & Sons, Ltd 01.11.2010
Wiley
Subjects
Activating Transcription Factor 6 - physiology
Animals
Biological and medical sciences
diabetes
Diabetes Mellitus - physiopathology
Diabetes Mellitus, Type 1 - physiopathology
Diabetes. Impaired glucose tolerance
DNA-Binding Proteins - physiology
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Endoplasmic Reticulum - physiology
Endoribonucleases - physiology
Epiphyses - abnormalities
Epiphyses - physiopathology
ER stress
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Fundamental and applied biological sciences. Psychology
General aspects
Glycoproteins - physiology
Humans
Insulin-Secreting Cells - cytology
Insulin-Secreting Cells - physiology
Islets of Langerhans - physiology
Medical sciences
Mice
Osteochondrodysplasias - physiopathology
PERK
Protein-Serine-Threonine Kinases - physiology
Regulatory Factor X Transcription Factors
Stress, Physiological - physiology
Transcription Factors - physiology
Unfolded Protein Response
UPR
Vertebrates: endocrinology
Endocrinopathy
Disease
Diabetes mellitus
UPR
ER stress
PERK
Endoplasmic reticulum
diabetes
Endocrinology
Stress
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Abstract Endoplasmic reticulum (ER) stress is an integral part of life for all professional secretory cells, but it has been studied to greatest depth in the pancreatic β‐cell. This reflects both the crucial role played by ER stress in the pathogenesis of diabetes and also the exquisite vulnerability of these cells to ER dysfunction. The adaptive cellular response to ER stress, the unfolded protein response, comprises mechanisms to both regulate new protein translation and a transcriptional program to allow adaptation to the stress. The core of this response is a triad of stress‐sensing proteins: protein kinase R‐like endoplasmic reticulum kinase (PERK), inositol‐requiring enzyme 1 (IRE1) and activating transcription factor 6. All three regulate portions of the transcriptional unfolded protein response, while PERK also attenuates protein synthesis during ER stress and IRE1 interacts directly with the c‐Jun amino‐terminal kinase stress kinase pathway. In this review we shall discuss these processes in detail, with emphasis given to their impact on diabetes and how recent findings indicate that ER stress may be responsible for the loss of β‐cell mass in the disease. Copyright © 2010 John Wiley & Sons, Ltd.
AbstractList Endoplasmic reticulum (ER) stress is an integral part of life for all professional secretory cells, but it has been studied to greatest depth in the pancreatic β-cell. This reflects both the crucial role played by ER stress in the pathogenesis of diabetes and also the exquisite vulnerability of these cells to ER dysfunction. The adaptive cellular response to ER stress, the unfolded protein response, comprises mechanisms to both regulate new protein translation and a transcriptional program to allow adaptation to the stress. The core of this response is a triad of stress-sensing proteins: protein kinase R-like endoplasmic reticulum kinase (PERK), inositol-requiring enzyme 1 (IRE1) and activating transcription factor 6. All three regulate portions of the transcriptional unfolded protein response, while PERK also attenuates protein synthesis during ER stress and IRE1 interacts directly with the c-Jun amino-terminal kinase stress kinase pathway. In this review we shall discuss these processes in detail, with emphasis given to their impact on diabetes and how recent findings indicate that ER stress may be responsible for the loss of β-cell mass in the disease.
Abstract Endoplasmic reticulum (ER) stress is an integral part of life for all professional secretory cells, but it has been studied to greatest depth in the pancreatic β‐cell. This reflects both the crucial role played by ER stress in the pathogenesis of diabetes and also the exquisite vulnerability of these cells to ER dysfunction. The adaptive cellular response to ER stress, the unfolded protein response, comprises mechanisms to both regulate new protein translation and a transcriptional program to allow adaptation to the stress. The core of this response is a triad of stress‐sensing proteins: protein kinase R‐like endoplasmic reticulum kinase (PERK), inositol‐requiring enzyme 1 (IRE1) and activating transcription factor 6. All three regulate portions of the transcriptional unfolded protein response, while PERK also attenuates protein synthesis during ER stress and IRE1 interacts directly with the c‐Jun amino‐terminal kinase stress kinase pathway. In this review we shall discuss these processes in detail, with emphasis given to their impact on diabetes and how recent findings indicate that ER stress may be responsible for the loss of β‐cell mass in the disease. Copyright © 2010 John Wiley & Sons, Ltd.
Endoplasmic reticulum (ER) stress is an integral part of life for all professional secretory cells, but it has been studied to greatest depth in the pancreatic β‐cell. This reflects both the crucial role played by ER stress in the pathogenesis of diabetes and also the exquisite vulnerability of these cells to ER dysfunction. The adaptive cellular response to ER stress, the unfolded protein response, comprises mechanisms to both regulate new protein translation and a transcriptional program to allow adaptation to the stress. The core of this response is a triad of stress‐sensing proteins: protein kinase R‐like endoplasmic reticulum kinase (PERK), inositol‐requiring enzyme 1 (IRE1) and activating transcription factor 6. All three regulate portions of the transcriptional unfolded protein response, while PERK also attenuates protein synthesis during ER stress and IRE1 interacts directly with the c‐Jun amino‐terminal kinase stress kinase pathway. In this review we shall discuss these processes in detail, with emphasis given to their impact on diabetes and how recent findings indicate that ER stress may be responsible for the loss of β‐cell mass in the disease. Copyright © 2010 John Wiley & Sons, Ltd.
Author Daly, Marie-Louise
Dalton, Lucy E.
Malzer, Elke
Thomas, Sally E.
Marciniak, Stefan J.
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Issue 8
Keywords Endocrinopathy
Disease
Diabetes mellitus
UPR
ER stress
PERK
Endoplasmic reticulum
diabetes
Endocrinology
Stress
Language English
License CC BY 4.0
Copyright © 2010 John Wiley & Sons, Ltd.
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– name: England
PublicationTitle Diabetes/metabolism research and reviews
PublicationTitleAlternate Diabetes Metab. Res. Rev
PublicationYear 2010
Publisher John Wiley & Sons, Ltd
Wiley
Publisher_xml – name: John Wiley & Sons, Ltd
– name: Wiley
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2009; 10
2000; 14
2007; 293
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2007; 8
2008; 118
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2000; 346
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2000; 74
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1998; 2
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1989; 57
2008; 132
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2005; 11
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2009; 106
2007; 148
2007; 303
2000; 6
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2008; 7
1972; 80
2000; 2
2009; 150
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2003; 11
2005; 24
2003; 99
2005; 25
2009; 52
1993; 73
1999; 19
2001; 292
2003; 3
2005; 307
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1997; 17
1999; 10
1999; 96
2000; 287
2002; 109
1996; 20
2001; 98
2007; 27
2006; 124
2004; 101
2007; 404
2002; 293
2004; 82
2000; 25
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2005; 433
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2002; 298
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2006; 3
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1994; 120
1988; 8
2002; 22
2005; 54
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Snippet Endoplasmic reticulum (ER) stress is an integral part of life for all professional secretory cells, but it has been studied to greatest depth in the pancreatic...
Abstract Endoplasmic reticulum (ER) stress is an integral part of life for all professional secretory cells, but it has been studied to greatest depth in the...
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SubjectTerms Activating Transcription Factor 6 - physiology
Animals
Biological and medical sciences
diabetes
Diabetes Mellitus - physiopathology
Diabetes Mellitus, Type 1 - physiopathology
Diabetes. Impaired glucose tolerance
DNA-Binding Proteins - physiology
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Endoplasmic Reticulum - physiology
Endoribonucleases - physiology
Epiphyses - abnormalities
Epiphyses - physiopathology
ER stress
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Fundamental and applied biological sciences. Psychology
General aspects
Glycoproteins - physiology
Humans
Insulin-Secreting Cells - cytology
Insulin-Secreting Cells - physiology
Islets of Langerhans - physiology
Medical sciences
Mice
Osteochondrodysplasias - physiopathology
PERK
Protein-Serine-Threonine Kinases - physiology
Regulatory Factor X Transcription Factors
Stress, Physiological - physiology
Transcription Factors - physiology
Unfolded Protein Response
UPR
Vertebrates: endocrinology
Title Diabetes as a disease of endoplasmic reticulum stress
URI https://api.istex.fr/ark:/67375/WNG-JN84CG7V-6/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fdmrr.1132
https://www.ncbi.nlm.nih.gov/pubmed/20922715
https://search.proquest.com/docview/762283212
Volume 26
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