Breakers of advanced glycation end products restore large artery properties in experimental diabetes.

@article{Wolffenbuttel1998BreakersOA,
  title={Breakers of advanced glycation end products restore large artery properties in experimental diabetes.},
  author={Bruce H. R. Wolffenbuttel and Chantal M Boulanger and Francy R L Crijns and Maya S P Huijberts and Pierre Poitevin and G N M Swennen and Sara Vasan and Judith J Egan and Peter Ulrich and Anthony Cerami and Bernard I L{\'e}vy},
  journal={Proceedings of the National Academy of Sciences of the United States of America},
  year={1998},
  volume={95 8},
  pages={4630-4}
}
Glucose and other reducing sugars react with proteins by a nonenzymatic, posttranslational modification process called nonenzymatic glycation. The formation of advanced glycation end products (AGEs) on connective tissue and matrix components accounts largely for the increase in collagen crosslinking that accompanies normal aging and which occurs at an accelerated rate in diabetes, leading to an increase in arterial stiffness. A new class of AGE crosslink "breakers" reacts with and cleaves these… CONTINUE READING

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