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Cited by 428

The DOI matches its Crossref record; 171 of the 171 references it cites were found in a registry or an index.

RAGE regulation and signaling in inflammation and beyond

Kierdorf, Katrin, Fritz, Günter·2013·Journal of Leukocyte Biology

Abstract

RAGE is a key molecule in the onset and sustainment of the inflammatory response. New studies indicate that RAGE might represent a new link between the innate and adaptive immune system. RAGE belongs to the superfamily of Ig cell-surface receptors and is expressed on all types of leukocytes promoting activation, migration, or maturation of the different cells. RAGE expression is prominent on the activated endothelium, where it mediates leukocyte adhesion and transmigration. Moreover, proinflammatory molecules released from the inflamed or injured vascular system induce migration and proliferation of SMCs. RAGE binds a large number of different ligands and is therefore considered as a PRR, recognizing a structural motif rather than a specific ligand. In this review, we summarize the current knowledge about the signaling pathways activated in the different cell types and discuss a potential activation mechanism of RAGE, as well as putative options for therapeutic intervention.

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Metadata

Authors
Kierdorf, K., & Fritz, G.
Venue
Journal of Leukocyte Biology
Published
2013-03-29
Volume
94
Issue
1
Pages
55-68
ISSN
  • 0741-5400 (ISSN-L)
  • 1938-3673
OpenAlex
W2105327109
Cited by
428
References
171
FWCI
11.38
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: RAGE regulation and signaling in inflammation and beyond. https://app.cochat.ai/papers/10.1189/jlb.1012519
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Kierdorf, K., & Fritz, G. (2013). RAGE regulation and signaling in inflammation and beyond. Journal of Leukocyte Biology. https://doi.org/10.1189/jlb.1012519

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.