RAGE does not contribute to renal injury and damage upon ischemia/reperfusion-induced injury.

@article{Dessing2012RAGEDN,
  title={RAGE does not contribute to renal injury and damage upon ischemia/reperfusion-induced injury.},
  author={Mark C Dessing and Wilco P. C. Pulskens and Gwendoline J D Teske and Loes Butter and Tom van der Poll and H. -S. Yang and Kevin J Tracey and Peter P Nawroth and Angelika Bierhaus and Sandrine Florquin and Jaklien C. Leemans},
  journal={Journal of innate immunity},
  year={2012},
  volume={4 1},
  pages={80-5}
}
The receptor for advanced glycation end products (RAGE) mediates a variety of inflammatory responses in renal diseases, but its role in renal ischemia/reperfusion (I/R) injury is unknown. We showed that during renal I/R, RAGE ligands HMGB1 and S100B are expressed. However, RAGE deficiency does not affect renal injury and function upon I/R-induced injury. 

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