RAGE Mediates a Novel Proinflammatory Axis
Open accessAbstract
S100/calgranulin polypeptides are present at sites of inflammation, likely released by inflammatory cells targeted to such loci by a range of environmental cues. We report here that receptor for AGE (RAGE) is a central cell surface receptor for EN-RAGE (extracellular newly identified RAGE-binding protein) and related members of the S100/calgranulin superfamily. Interaction of EN-RAGEs with cellular RAGE on endothelium, mononuclear phagocytes, and lymphocytes triggers cellular activation, with generation of key proinflammatory mediators. Blockade of EN-RAGE/RAGE quenches delayed-type hypersensitivity and inflammatory colitis in murine models by arresting activation of central signaling pathways and expression of inflammatory gene mediators. These data highlight a novel paradigm in inflammation and identify roles for EN-RAGEs and RAGE in chronic cellular activation and tissue injury.
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Activation of RAGE by its ligands upregulates inflammatory signalling pathways including NF-κB, phosphoinositide 3-kinase, JAK-STAT and MAPK, leading to induction of pro-inflammatory cytokines such as TNF.
“Activation of RAGe by its ligands results in the upregulation of several inflammatory signalling pathways, including, but not limited to, NF-κb, phospho inositide 3-kinase, Janus kinase (JAK)–signal transducer and activator of transcription (STAT) and MAPK signalling pathways, which lead to induction of pro-inflammatory cytokines such as TNF19,91,95,96.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [19]
RAGE recognizes S100 family members.
“In addition to AGes, RAGe also recognizes HMGb193 and the S100 family members19, which are released during cellular stress and necrotic cell death, and β-amyloid94, the accumulation of which is pathogenic in Alzheimer's disease.”
From Sterile inflammation: sensing and reacting to damage (2010) · cites this paper as [19]
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Cellular and molecular mechanisms of sarcopenia: The S100B perspective
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APPswe/Aβ regulation of osteoclast activation and RAGE expression in an age-dependent manner
Cui, S., Xiong, F., Hong, Y., Jung, J.-U., Li, X.-S., Liu, J.-Z., Yan, R., Mei, L., Feng, X., & Xiong, W.-C. (2011) · Journal of Bone and Mineral Research · doi:10.1002/jbmr.299 · Cited by 101 · see citing works
“Human Ab (1-42) (from AnaSpec, Fremont, CA, USA) was used.”
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RAGE mediates vascular injury and inflammation after global cerebral ischemia
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Self-citationArguing for the motion: yes, RAGE is a receptor for advanced glycation endproducts
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Inflammation: good or bad for ADHD?
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RAGE Signaling in Skeletal Biology
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Biomaterials-Driven Sterile Inflammation
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- Authors
- Hofmann, M. A., Drury, S., Fu, C., Qu, W., Taguchi, A., Lu, Y., Avila, C., Kambham, N., Bierhaus, A., Nawroth, P., Neurath, M. F., Slattery, T., Beach, D., McClary, J., Nagashima, M., Morser, J., Stern, D., & Schmidt, A. M.
- Affiliations
- Columbia University (US)
- University of Tübingen (DE)
- Johannes Gutenberg University Mainz (DE)
- Corresponding author
- Schmidt, Ann Marie
- ORCID
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 1999-06
- Volume
- 97
- Issue
- 7
- Pages
- 889-901
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2071675524
- Cited by
- 1,864
- References
- 43
- Citations by year
- 2026: 27 · 2025: 41 · 2024: 51 · 2023: 41 · 2022: 70 · 2021: 67 · 2020: 49 · 2019: 68 · 2018: 62 · 2017: 59 · 2016: 80 · 2015: 90 · 2014: 96 · 2013: 92 · 2012: 99
- FWCI
- 28.37
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cell (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (1r01hl056881-01, 1r01dk052495-01)
- U.S. Public Health Service
- National Heart, Lung, and Blood Institute (P01HL060901, HL 56881, HL60901)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK52495)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › S100 Proteins and Annexins
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Keywords
- receptor for advanced glycation end products, RAGE, S100A12, pro-inflammatory signaling, delayed-type hypersensitivity, inflammatory colitis, endothelial activation, mononuclear phagocytes, lymphocytes, tissue damage
- MeSH terms
- S100A12 Protein, Receptor for Advanced Glycation End Products, Amino Acid Sequence, Animals, Base Sequence, Cattle, Colitis, Endothelium, Vascular, Female, Humans, Leukocytes, Mononuclear, Membrane Proteins, Mice, Inbred C57BL, Molecular Sequence Data, S100 Proteins, Peptides, Phagocytes, Receptors, Immunologic, DNA, Complementary, Jurkat Cells, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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