PS3 - 14. Glyoxalase-I overexpression partially prevents diabetes-induced impaired arteriogenesis in a rat hind limb ischemia model
| Autor: | Coen D.A. Stehouwer, Casper G. Schalkwijk, Mark J. Post, Walter H. Backes, Liang Yu, Jos Slenter, Allard Wagenaar, Olaf Brouwers, Maya S. P. Huijberts, Petra Niessen |
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| Rok vydání: | 2011 |
| Předmět: |
chemistry.chemical_classification
medicine.medical_specialty biology business.industry Methylglyoxal medicine.disease chemistry.chemical_compound Lactoylglutathione lyase Endocrinology medicine.anatomical_structure Enzyme chemistry Glycation Diabetes mellitus Internal medicine biology.protein Medicine Arteriogenesis business Intracellular Artery |
| Zdroj: | Nederlands Tijdschrift voor Diabetologie. 9:99-100 |
| ISSN: | 1876-6242 1567-2743 |
| DOI: | 10.1007/s12467-011-0039-y |
| Popis: | Arteriogenesis is an important mechanism in improving the outcome of ischemic vascular diseases. However in patients who suffer from diabetes, this compensational collateral capacity is impaired. Hyperglycemia is the initial factor of diabetes induced vascular damage, but the mechanisms involved are poorly understood. The advanced glycation endproduct (AGE) precursor methylglyoxal (MGO) is a highly reactive oxo-aldehyde, which can be detoxified by the enzyme glyoxalase-I. We hypothesized that the reduced collateral artery remodeling capacity in diabetes is, at least partially, caused by intracellular glycation and defective regulation of the GLO-I enzyme. |
| Databáze: | OpenAIRE |
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