Cited by 193Endoplasmic Reticulum Stress and DiseaseMetabolism, Diabetes, and CancerPancreatic function and diabetes

Oxidative stress, ER stress, and the JNK pathway in type 2 diabetes

Kaneto, Hideaki, Matsuoka, Taka-aki, Nakatani, Yoshihisa, Kawamori, Dan, Miyatsuka, Takeshi, Matsuhisa, Munehide, Yamasaki, Yoshimitsu·2005·Journal of Molecular Medicine

Abstract

Pancreatic beta-cell dysfunction and insulin resistance are observed in type 2 diabetes. Under diabetic conditions, oxidative stress and ER stress are induced in various tissues, leading to activation of the JNK pathway. This JNK activation suppresses insulin biosynthesis and interferes with insulin action. Indeed, suppression of the JNK pathway in diabetic mice improves insulin resistance and ameliorates glucose tolerance. Thus, the JNK pathway plays a central role in pathogenesis of type 2 diabetes and may be a potential target for diabetes therapy.

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Crossref · 10.1007/s00109-005-0640-x

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108 of 108 references verified0 citation errors · 0 not checkable

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Authors
Kaneto, H., Matsuoka, T.-A., Nakatani, Y., Kawamori, D., Miyatsuka, T., Matsuhisa, M., & Yamasaki, Y.
Affiliations
The University of Osaka (JP)
Corresponding author
Kaneto, Hideaki
Venue
Journal of Molecular Medicine
Published
2005-03-10
Volume
83
Issue
6
Pages
429-439
ISSN
  • 0946-2716 (ISSN-L)
  • 1432-1440
OpenAlex
W2027604252
Cited by
193
References
108
Citations by year
2026: 3 · 2025: 4 · 2024: 7 · 2023: 9 · 2022: 4 · 2021: 7 · 2020: 12 · 2019: 10 · 2018: 9 · 2017: 8 · 2016: 5 · 2015: 6 · 2014: 8 · 2013: 17 · 2012: 12
FWCI
5.69
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Molecular Medicine (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Endoplasmic Reticulum Stress and Disease
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
type 2 diabetes, oxidative stress, endoplasmic reticulum stress, JNK signaling, beta-cell dysfunction, insulin resistance, insulin biosynthesis, glucose tolerance, diabetes treatment
MeSH terms
Animals, Diabetes Mellitus, Type 2, Endoplasmic Reticulum, Islets of Langerhans, Signal Transduction, Oxidative Stress, JNK Mitogen-Activated Protein Kinases, Mice

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