Cited by 151Endoplasmic Reticulum Stress and DiseasePancreatic function and diabetesIon Channels and Receptors

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Endoplasmic Reticulum Stress and Diabetes Mellitus.

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ARAKI, Eiichi, OYADOMARI, Seiichi, MORI, Masataka·2003·Internal Medicine

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Abstract

Pancreatic beta-cells are strongly engaged in protein secretion and have highly developed endoplasmic reticulum (ER). Proper folding of polypeptide into a three-dimensional structure is essential for cellular function and protein malfolding can threaten cell survival. Various conditions can perturb the protein folding in the ER, which is collectively called ER stress. In order to adapt ER stress conditions, the cells respond in three distinct ways such as transcriptional induction of ER chaperones, translational attenuation, and ER-associated degradation (ERAD). However, when ER functions are severely impaired, the cell is eliminated by apoptosis via transcriptional induction of CHOP/GADD153, the activation of cJUN NH2-terminal kinase, and/or the activation of caspase-12. Recent studies have revealed that beta-cell is one of the most susceptible cells for ER stress, and ER stress-mediated apoptosis in beta-cells can be a cause of diabetes. A comprehensive understanding of the impact of the ER stress pathway in beta-cells and how it relates to the development of diabetes may contribute to provide new targets for the prevention and treatment of this disease.

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Authors: ARAKI, E., OYADOMARI, S., & MORI, M.
Affiliations: Kumamoto University (JP)
ORCID: ARAKI, Eiichi
OYADOMARI, Seiichi
MORI, Masataka
Venue: Internal Medicine
Publisher: Japanese Society of Internal Medicine
Published: 2003
Volume: 42
Issue: 1
Pages: 7-14
ISSN: 0918-2918 (ISSN-L)
1349-7235
DOI: 10.2169/internalmedicine.42.7
OpenAlex: W2056689556
Cited by: 151
References: 55
Citations by year: 2025: 1 · 2024: 2 · 2023: 2 · 2022: 4 · 2021: 4 · 2020: 4 · 2019: 2 · 2018: 8 · 2017: 7 · 2016: 4 · 2015: 10 · 2014: 8 · 2013: 8 · 2012: 10
FWCI: 0.37
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Internal Medicine (publishedVersion)
PubMed (publishedVersion)
Funders: Ministry of Education, Culture, Sports, Science and Technology
Japan Society for the Promotion of Science (14370339)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
Life Sciences › Neuroscience › Sensory Systems › Ion Channels and Receptors
Keywords: endoplasmic reticulum stress, diabetes mellitus, pancreatic beta cells, protein folding, ER-associated degradation, CHOP/GADD153, c-Jun N-terminal kinase, caspase-12, beta-cell apoptosis, ER chaperones, translational attenuation
MeSH terms: Amyloid, Animals, Diabetes Mellitus, Endoplasmic Reticulum, Humans, Islets of Langerhans, Mice, Mutant Strains, Models, Biological, Nitric Oxide, Eukaryotic Initiation Factor-2, Apoptosis, Protein Folding, eIF-2 Kinase, Mice

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Endoplasmic Reticulum Stress and Diabetes Mellitus.

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