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Title: RAGE does not contribute to renal injury and damage upon ischemia/reperfusion-induced injury.
Author(s): Dessing, M.C.; Pulskens, W.P.C.; Teske, G.J.; Butter, L.M.; Poll, T. van der; Yang, H.; Tracey, K.J.; Nawroth, P.P.; Bierhaus, A.; Florquin, S.; Leemans, J.C.
Publication year: 2012
Source: Journal of Innate Immunity, vol. 4, iss. 1, (2012), pp. 80-85
ISSN: 1662-811X
DOI: https://doi.org/10.1159/000334251
Publication type: Article / Letter to editor

Please use this identifier to cite or link to this item : http://hdl.handle.net/2066/109256   http://hdl.handle.net/2066/109256

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Subject: NCMLS 5: Membrane transport and intracellular motility IGMD 9: Renal disorder
ONCOL 3: Translational research
Organization: Physiology
Pathology
Journal title:
Journal of Innate Immunity
Volume: vol. 4
Issue: iss. 1
Page start: p. 80
Page end: p. 85
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.

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