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Hamostaseologie 2001; 21(04): 151-158
DOI: 10.1055/s-0037-1619518
Original article
Schattauer GmbH

Endothelzellaktivierung bei Diabetes mellitus

Endothelial cell activation in diabetes mellitus
A. Bierhaus
1   Medizinische Klinik I, Universität Heidelberg
,
M. Andrassy
1   Medizinische Klinik I, Universität Heidelberg
,
S. Schiekofer
1   Medizinische Klinik I, Universität Heidelberg
,
J. Chen
1   Medizinische Klinik I, Universität Heidelberg
,
P. M. Humpert
1   Medizinische Klinik I, Universität Heidelberg
4   Deutsches Herzzentrum München, Abt. für experimentelle Kardiologie
,
L. Bai
1   Medizinische Klinik I, Universität Heidelberg
3   Chinese Academy of Medical Sciences, Peking Union Medical College, Department of Biochemistry, China
,
B. Chen
3   Chinese Academy of Medical Sciences, Peking Union Medical College, Department of Biochemistry, China
,
E. Schleicher
2   Medizinische Klinik IV, Universität Tübingen
,
P. P. Nawroth
1   Medizinische Klinik I, Universität Heidelberg
› Author Affiliations
Further Information

Publication History

Publication Date:
27 December 2017 (online)

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Zusammenfassung

Gefäßerkrankungen gelten als eine Hauptursache für die Morbidität und Mortalität von Patienten mit Diabetes mellitus. Klinische Studien zeigen, dass eine intensivierte Blutzuckerkontrolle die Entwicklung vaskulärer Spätschäden deutlich verlangsamt, sodass Hyperglykämie mittlerweile als ein wichtiger Faktor für die Enstehung von Gefäßveränderungen betrachtet wird. Verschiedene durch Hyperglykämie aktivierte Stoffwechselwege wie der Polyolstoffwechselweg, die Aktivierung der Proteinkinase C, die nicht-enzymatische Glykierung von Proteinen und Veränderungen im Redoxpotenzial beeinflussen und verstärken sich dabei gegenseitig. Eine mögliche gemeinsame Endstrecke aller durch Hyperglykämie bedingten zellulären Veränderungen ist die Erzeugung von reaktiven Sauerstoffmolekülen (ROIs) und von oxidativem Stress. Oxidativer Stress aktiviert den Transkriptionsfaktor NF-κB und in Folge die NF-κB-abhängige endotheliale Genexpression, die möglicherweise zur endothelialen Dysfunktion bei Diabetes mellitus beitragen kann.

Summary

Vascular complications are regarded as a main cause for the morbidity and mortality in diabetes mellitus. Clinical studies demonstrate that intensive glycaemic control seems to slow the onset and progression of vascular complications and indicate that hyperglycaemia is one important mediator of endothelial dysfunction. Various pathways as the polyol pathway, activation of protein kinase C, formation of advanced glycation endproducts (AGEs) and changes in the redox potential are supposed to contribute to the adverse effects of hyperglycaemia on the endothelium. A common endpoint of hyperglycaemia dependent cellular changes is the generation of reactive oxygen intermediates (ROIs) and the presence of elevated oxidative stress, that results in activation of the transcription factor NF-κB and alterations in endothelial gene expression that might contribute to endothelial dysfunction in diabetes mellitus.

Schlüsselwörter

Nicht-enzymatische Glykierung - RAGE - oxidativer Stress - NF-κB

Keywords

Advanced glycation endproducts - RAGE - oxidative stress - NF-κB
 

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