Endoplasmic Reticulum Stress and Diabetes Mellitus.

DOI Web Site Web Site PubMed 被引用文献6件 参考文献51件
  • ARAKI Eiichi
    Departments of Metabolic Medicine, Kumamoto University School of Medicine
  • OYADOMARI Seiichi
    Departments of Metabolic Medicine, Kumamoto University School of Medicine Departments of Molecular Genetics, Kumamoto University School of Medicine
  • MORI Masataka
    Departments of Molecular Genetics, Kumamoto University School of Medicine

この論文をさがす

説明

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.<br>(Internal Medicine 42: 7-14, 2003)

収録刊行物

  • Internal Medicine

    Internal Medicine 42 (1), 7-14, 2003

    一般社団法人 日本内科学会

被引用文献 (6)*注記

もっと見る

参考文献 (51)*注記

もっと見る

キーワード

詳細情報 詳細情報について

問題の指摘

ページトップへ