The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
The role of oxidative stress in the onset and progression of diabetes and its complications: asummary of a Congress Series sponsored byUNESCO-MCBN, the American Diabetes Association and the German Diabetes Society
Open accessAbstract
This review summarises the results and discussions of an UNESCO-MCBN supported symposium on oxidative stress and its role in the onset and progression of diabetes. There is convincing experimental and clinical evidence that the generation of reactive oxygen species (ROI) is increased in both types of diabetes and that the onset of diabetes is closely associated with oxidative stress. Nevertheless there is controversy about which markers of oxidative stress are most reliable and suitable for clinical practice. There are various mechanisms that contribute to the formation of ROI. It is generally accepted that vascular cells and especially the endothelium become one major source of ROI. An important role of oxidative stress for the development of vascular and neurological complications is suggested by experimental and clinical studies. The precise mechanisms by which oxidative stress may accelerate the development of complications in diabetes are only partly known. There is however evidence for a role of protein kinase C, advanced glycation end products (AGE) and activation of transcription factors such as NF kappa B, but the exact signalling pathways and the interactions with ROI remain a matter of discussion. Additionally, results of very recent studies suggest a role for ROI in the development of insulin resistance. ROI interfere with insulin signalling at various levels and are able to inhibit the translocation of GLUT4 in the plasma membrane. Evidence for a protective effect of antioxidants has been presented in experimental studies, but conclusive evidence from patient studies is missing. Large-scale clinical trials such as the DCCT Study or the UKPDS Study are needed to evaluate the long-term effects of antioxidants in diabetic patients and their potential to reduce the medical and socio-economic burden of diabetes and its complications.
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Cites
Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damage
Nishikawa, T., Edelstein, D., Du, X. L., Yamagishi, S.-I., Matsumura, T., Kaneda, Y., Yorek, M. A., Beebe, D., Oates, P. J., Hammes, H.-P., et al. (2000) · Nature · doi:10.1038/35008121 · Cited by 4,277
Protein kinase C and lipid signaling for sustained cellular responses
Nishizuka, Y. (1995) · The FASEB Journal · doi:10.1096/fasebj.9.7.7737456 · Cited by 2,499
Stephens, N. G., Parsons, A., Brown, M. J., Schofield, P. M., Kelly, F., Cheeseman, K., & Mitchinson, M. (1996) · The Lancet · doi:10.1016/s0140-6736(96)90866-1 · Cited by 2,148
Hypercholesterolemia increases endothelial superoxide anion production.
Ohara, Y., Peterson, T. E., & Harrison, D. G. (1993) · Journal of Clinical Investigation · doi:10.1172/jci116491 · Cited by 1,765 · cited 1×
“In which ways may ROI affect the regulation of blood flow? There is considerable evidence that nitric oxide reacts in a diffusion-controlled way with superoxide anions to peroxynitrite [215].”
BackgroundDyck, P. J., Kratz, K. M., Karnes, J. L., Litchy, W. J., Klein, R., Pach, J. M., Wilson, D. M., O'Brien, P. C., & Melton, L. J. (1993) · Neurology · doi:10.1212/wnl.43.4.817 · Cited by 1,482
Pirart, J. (1978) · Diabetes Care · doi:10.2337/diacare.1.3.168 · Cited by 1,290
Kawano, H., Motoyama, T., Hirashima, O., Hirai, N., Miyao, Y., Sakamoto, T., Kugiyama, K., Ogawa, H., & Yasue, H. (1999) · Journal of the American College of Cardiology · doi:10.1016/s0735-1097(99)00168-0 · Cited by 676
Diabetes mellitus and free radicals
Wolff, S. P. (1993) · British Medical Bulletin · doi:10.1093/oxfordjournals.bmb.a072637 · Cited by 660
The Effect of Intensive Diabetes Therapy on the Development and Progression of Neuropathy
The Diabetes Control and Complications Trial Research Group. (1995) · Annals of Internal Medicine · doi:10.7326/0003-4819-122-8-199504150-00001 · Cited by 602
Ziegler, D., Hanefeld, M., Ruhnau, K. J., Mei\ner, H. P., Lobisch, M., Sch�tte, K., Gries, F. A., & The ALADIN Study Group (1995) · Diabetologia · doi:10.1007/bf00400603 · Cited by 525
What nitrates tyrosine? Is nitrotyrosine specific as a biomarker of peroxynitrite formation in vivo?
Halliwell, B. (1997) · FEBS Letters · doi:10.1016/s0014-5793(97)00469-9 · Cited by 472
Bursell, S. E., Clermont, A. C., Aiello, L. P., Aiello, L. M., Schlossman, D. K., Feener, E. P., Laffel, L., & King, G. L. (1999) · Diabetes Care · doi:10.2337/diacare.22.8.1245 · Cited by 333
Self-citationMetabolic and Vascular Factors in the Pathogenesis of Diabetic Neuropathy
Cameron, N. E., & Cotter, M. A. (1997) · Diabetes · doi:10.2337/diab.46.2.s31 · Cited by 312
Relationships between plasma measures of oxidative stress and metabolic control in NIDDM
Nourooz-Zadeh, J., Rahimi, A., Tajaddini-Sarmadi, J., Tritschler, H., Rosen, P., Halliwell, B., & Betteridge, D. J. (1997) · Diabetologia · doi:10.1007/s001250050729 · Cited by 303
Self-citationJacob, S., Ruus, P., Hermann, R., Tritschler, H. J., Maerker, E., Renn, W., Augustin, H. J., Dietze, G. J., & Rett, K. (1999) · Free Radical Biology and Medicine · doi:10.1016/s0891-5849(99)00089-1 · Cited by 280
Self-citationCameron, N. E., & Cotter, M. A. (1995) · Journal of Clinical Investigation · doi:10.1172/jci118104 · Cited by 147
Cited by
Oxidative Stress and Stress-Activated Signaling Pathways: A Unifying Hypothesis of Type 2 Diabetes
Evans, J. L., Goldfine, I. D., Maddux, B. A., & Grodsky, G. M. (2002) · Endocrine Reviews · doi:10.1210/er.2001-0039 · Cited by 2,232
Evans, J. L., Goldfine, I. D., Maddux, B. A., & Grodsky, G. M. (2003) · Diabetes · doi:10.2337/diabetes.52.1.1 · Cited by 1,482
Hassan, M. M., Hwang, L.-Y., Hatten, C. J., Swaim, M., Li, D., Abbruzzese, J. L., Beasley, P., & Patt, Y. Z. (2002) · Hepatology · doi:10.1053/jhep.2002.36780 · Cited by 762
The Molecular Basis for Oxidative Stress-Induced Insulin Resistance
Evans, J. L., Maddux, B. A., & Goldfine, I. D. (2005) · Antioxidants & Redox Signaling · doi:10.1089/ars.2005.7.1040 · Cited by 587
Molecular pathways associated with oxidative stress in diabetes mellitus
Ighodaro, O. M. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.09.058 · Cited by 555
Metadata
- Authors
- R�sen, P., Nawroth, P. P., King, G., M�ller, W., Tritschler, H.-J., & Packer, L.
- Venue
- Diabetes/Metabolism Research and Reviews
- Publisher
- Wiley
- Published
- 2001
- Volume
- 17
- Issue
- 3
- Pages
- 189-212
- ISSN
- 1520-7552 (ISSN-L)
- 1520-7560
- OpenAlex
- W1976422365
- Cited by
- 887
- References
- 17
- FWCI
- 21.68
- Type
- journal article
- Language
- en
- Open access
- bronze
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