The DOI matches its Crossref record; 21 of the 21 references it cites were found in a registry or an index.
Involvement of Oxidative Stress in the Pathogenesis of Diabetes
Abstract
Pancreatic beta-cell failure is the common characteristic of type 1 and type 2 diabetes. Type 1 diabetes is induced by pancreatic beta-cell destruction, which is mediated by an autoimmune mechanism and consequent inflammatory process. Various inflammatory cytokines and oxidative stress produced by islet-infiltrating immune cells have been proposed to play an important role in mediating the destruction of beta cells. The JNK pathway is also activated by such cytokines and oxidative stress and is involved in beta-cell destruction. Type 2 diabetes is the most prevalent and serious metabolic disease affecting people all over the world. Pancreatic beta-cell dysfunction and insulin resistance are the hallmark of type 2 diabetes. Once hyperglycemia becomes apparent, beta-cell function gradually deteriorates, and insulin resistance is aggravated. This process is called "glucose toxicity." Under such conditions, oxidative stress is provoked, and the JNK pathway is activated, which is likely involved in pancreatic beta-cell dysfunction and insulin resistance. In addition, oxidative stress and activation of the JNK pathway are involved in the progression of atherosclerosis, which is often observed under diabetic conditions. Taken together, it is likely that oxidative stress and subsequent activation of the JNK pathway are involved in the pathogenesis of type 1 and type 2 diabetes.
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Citations
Cites
Inflammation, stress, and diabetes
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A central role for JNK in obesity and insulin resistance
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Role of oxidative stress in diabetic complications: a new perspective on an old paradigm.
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Oxidative Stress and Stress-Activated Signaling Pathways: A Unifying Hypothesis of Type 2 Diabetes
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Oxidative Stress and Vascular Disease
Madamanchi, N. R., Vendrov, A., & Runge, M. S. (2005) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/01.atv.0000150649.39934.13 · Cited by 1,618 · cited 1×
“Taken together, activation of the JNK pathway triggers VSMC proliferation, leading to neointimal formation, and the JNK pathway could be a new therapeutic target for atherosclerosis (cid:5) (cid:5) Activation of the JNK pathway was closely correlated with the presence of clearly established plaques…”
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Fatty acid-induced β cell apoptosis: A link between obesity and diabetes
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Cited by
Tannins: Current knowledge of food sources, intake, bioavailability and biological effects
Serrano, J., Puupponen‐Pimiä, R., Dauer, A., Aura, A., & Saura‐Calixto, F. (2009) · Molecular Nutrition & Food Research · doi:10.1002/mnfr.200900039 · Cited by 810
Diabetes and Kidney Disease: Role of Oxidative Stress
Jha, J. C., Banal, C., Chow, B. S. M., Cooper, M. E., & Jandeleit-Dahm, K. (2016) · Antioxidants & Redox Signaling · doi:10.1089/ars.2016.6664 · Cited by 660
Molecular Mechanisms and Clinical Implications of Reversible Protein S -Glutathionylation
Mieyal, J. J., Gallogly, M. M., Qanungo, S., Sabens, E. A., & Shelton, M. D. (2008) · Antioxidants & Redox Signaling · doi:10.1089/ars.2008.2089 · Cited by 523
Sedeek, M., Callera, G., Montezano, A., Gutsol, A., Heitz, F., Szyndralewiez, C., Page, P., Kennedy, C. R. J., Burns, K. D., Touyz, R. M., et al. (2010) · American Journal of Physiology-Renal Physiology · doi:10.1152/ajprenal.00028.2010 · Cited by 396
JNK1 and IKKβ: molecular links between obesity and metabolic dysfunction
Solinas, G., & Karin, M. (2010) · The FASEB Journal · doi:10.1096/fj.09-151340 · Cited by 347
Metadata
- Authors
- Kaneto, H., Katakami, N., Kawamori, D., Miyatsuka, T., Sakamoto, K., Matsuoka, T.-A., Matsuhisa, M., & Yamasaki, Y.
- Venue
- Antioxidants & Redox Signaling
- Publisher
- SAGE Publications
- Published
- 2007-03
- Volume
- 9
- Issue
- 3
- Pages
- 355-366
- ISSN
- 1523-0864 (ISSN-L)
- 1557-7716
- OpenAlex
- W1996318348
- Cited by
- 263
- References
- 21
- FWCI
- 20.18
- Type
- journal article
- Language
- en
- Open access
- closed
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