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PS3 - 14. Glyoxalase-I overexpression partially prevents diabetes-induced impaired arteriogenesis in a rat hind limb ischemia model

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Nederlands Tijdschrift voor Diabetologie Aims and scope

Abstract

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.

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Authors and Affiliations

  1. Department of Internal Medicine, Maastricht University, Maastricht, The Netherlands

    Liang Yu, Olaf Brouwers, Petra Niessen, Coen Stehouwer, Maya Huijberts & Casper Schalkwijk

  2. Department of Radiology, Maastricht University, Maastricht, The Netherlands

    Jos Slenter & Walter Backes

  3. Department of Physiology,, Maastricht University, Maastricht, The Netherlands

    Allard Wagenaar & Mark Post

Authors
  1. Liang Yu
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  2. Olaf Brouwers
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  3. Petra Niessen
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  4. Jos Slenter
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  5. Allard Wagenaar
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  6. Mark Post
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  7. Walter Backes
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  8. Coen Stehouwer
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  9. Maya Huijberts
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  10. Casper Schalkwijk
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Additional information

1Department of Internal Medicine, Maastricht University, 2Department of Radiology, Maastricht University, 3Department of Physiology, Maastricht University. E-mail: olaf.brouwers@maastrichtuniversity.nl

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Yu, L., Brouwers, O., Niessen, P. et al. PS3 - 14. Glyoxalase-I overexpression partially prevents diabetes-induced impaired arteriogenesis in a rat hind limb ischemia model. NED. TIJDSCHR. DIABET. 9, 99–100 (2011). https://doi.org/10.1007/s12467-011-0039-y

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  • DOI: https://doi.org/10.1007/s12467-011-0039-y

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