RAGE does not contribute to renal injury and damage upon ischemia/reperfusion-induced injury
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 a...
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| Main Authors: | , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
2012
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| In: |
Journal of innate immunity
Year: 2012, Volume: 4, Issue: 1, Pages: 80-85 |
| ISSN: | 1662-8128 |
| DOI: | 10.1159/000334251 |
| Online Access: | Verlag, Volltext: http://dx.doi.org/10.1159/000334251 Verlag, Volltext: https://www.karger.com/Article/FullText/334251 
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| Author Notes: | Mark C. Dessing, Wilco P. Pulskens, Gwendoline J. Teske, Loes M. Butter, Tom van der Poll, Huan Yang, Kevin J. Tracey, Peter P. Nawroth, Angelika Bierhaus, Sandrine Florquin, Jaklien C. Leemans |
| Summary: | 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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| Item Description: | Published online: November 4, 2011 Gesehen am 11.12.2018 |
| Physical Description: | Online Resource |
| ISSN: | 1662-8128 |
| DOI: | 10.1159/000334251 |