The role of autophagy in pancreatitis

DOI 31 References
  • OHMURAYA Masaki
    Institute of Resource Development and Analysis, Kumamoto University

Bibliographic Information

Other Title
  • 膵炎とオートファジー

Abstract

Autophagy (cellular self-digestion) is a cellular pathway involved in protein and organelle degradation, and its deregulation is associated with several human diseases such as cancer, neurodegeneration, microbial infection and chronic inflammation. We previously showed that autophagy causes trypsinogen activation in pancreatic acinar cells, leading to acute pancreatitis. Recent studies showed that large vacuoles derived from autophagy, and p62/SQSTM1 (p62) aggregates occur in the acinar cells of genetically engineered mice models of chronic pancreatitis. p62 is a not only selective substrate for autophagy, but also a scaffold protein that has several functions in signal transduction, cell proliferation, cell survival, cell death, inflammation, tumorigenesis, and oxidative stress response. These novel data indicate that autophagy is impaired in chronic pancreatitis, and p62 deposition provokes chronic pancreatitis. These data should provide insight into novel molecular targets and therapeutic strategies for treatment of acute and chronic pancreatitis.<br>

Journal

  • Suizo

    Suizo 29 (1), 32-37, 2014

    Japan Pancreas Society

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Keywords

Details 詳細情報について

  • CRID
    1390282679616825600
  • NII Article ID
    130004496047
  • DOI
    10.2958/suizo.29.32
  • ISSN
    18812805
    09130071
  • Text Lang
    ja
  • Data Source
    • JaLC
    • Crossref
    • CiNii Articles
  • Abstract License Flag
    Disallowed

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