Endoplasmic Reticulum Stress and Diabetes Mellitus
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概要
- 論文の詳細を見る
Pancreatic β-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 β-cell is one of the most susceptible cells for ER stress, and ER stress-mediated apoptosis in β-cells can be a cause of diabetes. A comprehensive understanding of the impact of the ER stress pathway in β-cells and how it relates to the development of diabetes may contribute to provide new targets for the prevention and treatment of this disease.(Internal Medicine 42: 7-14, 2003)
- 社団法人 日本内科学会の論文
- 2003-01-01
著者
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Araki Eiichi
Department of Metabolic Medicine, Faculty of Life Sciences, Kumamoto University, Japan
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Araki Eiichi
Department Of Metabolic Medicine Faculty Of Medical And Pharmaceutical Sciences Kumamoto University
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Mori Masataka
Department Of Molecular Genetics Kumamoto University School Of Medicine
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Mori Masataka
Department Of Electrical Engineering Nagaoka University Of Technology
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OYADOMARI Seiichi
Department of Molecular Genetics, Graduate School of Medical Sciences, Kumamoto University
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Oyadomari Seiichi
Department Of Metabolic Medicine Kumamoto University School Of Medicine
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Araki Eiichi
Department Of Metabolic Medicine Faculty Of Life Sciences Kumamoto University
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