Molecular mechanisms of diabetic angiopathy--clues for innovative therapeutic interventions.
Advanced glycation end products (AGEs), known to accumulate during aging and at accelerated rate during the course of diabetes, have been demonstrated to induce changes in endothelial properties that might contribute to the pathogenesis of micro- and macroangiopathy. Since AGE-formation not only changes the physicochemical properties of proteins, but also induces cellular signalling, activation of transcription factors and subsequent gene expression, AGEs are now regarded as important mediators of diabetic vascular disease. The growing knowledge on the molecular mechanisms underlying the AGE-dependent activation of vascular endothelial cells implicates possible new therapeutic interventions in the therapy of diabetic angiopathy.
Medizinische Klinik I der Universität Heidelberg, Deutschland.
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Bierhaus
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Ziegler
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Nawroth
D003925:Diabetic Angiopathies / Q000188:drug therapy* / Q000209:etiology* / Q000378:metabolism; D004730:Endothelium, Vascular / Q000502:physiology; D017127:Glycation End Products, Advanced / Q000037:antagonists & inhibitors / Q000378:metabolism / Q000502:physiology; D006801:Humans; D016328:NF-kappa B / Q000502:physiology; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000037:antagonists & inhibitors / Q000235:genetics / Q000502:physiology
D017127:Glycation End Products, Advanced; D016328:NF-kappa B; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic