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


ABSTRACT: 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.

SUBMITTER: Dessing MC 

PROVIDER: S-EPMC8336648 | biostudies-literature | 2012

REPOSITORIES: biostudies-literature

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

Dessing Mark C MC   Pulskens Wilco P WP   Teske Gwendoline J GJ   Butter Loes M LM   van der Poll Tom T   Yang Huan H   Tracey Kevin J KJ   Nawroth Peter P PP   Bierhaus Angelika A   Florquin Sandrine S   Leemans Jaklien C JC  

Journal of innate immunity 20111104 1


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. ...[more]

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