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Verfasst von:Abdel-Khalek, Mohamed [VerfasserIn]   i
 Bierhaus, Angelika [VerfasserIn]   i
 Schiekofer, Stephan [VerfasserIn]   i
 Tritschler, Hans [VerfasserIn]   i
 Ziegler, Reinhard [VerfasserIn]   i
 Nawroth, Peter Paul [VerfasserIn]   i
Titel:The role of oxidative stress and NF-κB activation in late diabetic complications
Verf.angabe:Abdel Khalek Mohamed, Angelika Bierhaus, Stephan Schiekofer, Hans Tritschler, Reinhard Ziegler and Peter P. Nawroth
Jahr:1999
Umfang:11 S.
Fussnoten:Elektronische Reproduktion der Druck-Ausgabe ; First published: 16 December 2008 ; Gesehen am 12.05.2021
Titel Quelle:Enthalten in: Biofactors
Ort Quelle:Malden, Mass. : Wiley, 1997
Jahr Quelle:1999
Band/Heft Quelle:10(1999), 2/3, Seite 157-167
ISSN Quelle:1872-8081
Abstract:A common endpoint of hyperglycemia dependent cellular changes is the generation of reactive oxygen intermediates (ROIs) and the presence of elevated oxidative stress. Therefore, oxidative stress is supposed to play an important role in the development of late diabetic complications. Formation of advanced glycation end products (AGE's) due to elevated nonenzymatic glycation of proteins, lipids and nucleic acids is accompanied by oxidative, radical-generating reactions and thus represents a major source for oxygen free radicals under hyperglycemic conditions. Once formed, AGE's can influence cellular function by binding to several binding sites including the receptor for AGE's, RAGE. Binding of AGE's (and other ligands) to RAGE results in generation of intracellular oxidative stress and subsequent activation of the redox-sensitive transcription factor NF-κB in vitro and in vivo. Consistently, activation of NF-κB in diabetic patients correlates with the quality of glycemic control and can be reduced by treatment with the antioxidant α-lipoic acid. The development of techiques allowing for a tissue culture independent measurement of NF-κB activation in patients with diabetes mellitus gives insights into the molecular mechanisms linking diabetes mellitus and hyperglycemia with formation of advanced glycated endproducts and generation of oxidative stress finally resulting in oxidative stress mediated cellular activation.
DOI:doi:10.1002/biof.5520100211
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1002/biof.5520100211
 Volltext: https://iubmb.onlinelibrary.wiley.com/doi/abs/10.1002/biof.5520100211
 DOI: https://doi.org/10.1002/biof.5520100211
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1757713794
Verknüpfungen:→ Zeitschrift

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