The Receptor for Advanced Glycation Endproducts (RAGE) and Mediation of Inflammatory Neurodegeneration
Open accessAbstract
The Receptor for Advanced Glycation Endproducts (RAGE) is an immunoglobulin-type, transmembrane receptor that is expressed on numerous cell types in the Central Nervous System (CNS) and periphery, such as neurons, astrocytes, microglia, mononuclear phagocytes, epithelial cells and endothelial cells (ECs). RAGE binds a discrete repertoire of ligands, including non-enzymatically glycated proteins and lipids, also known as advanced glycation endproducts (AGEs), for which the receptor is named, in addition to multiple members of the S100/calgranulin family, oligomeric forms of Aβ, high mobility group box 1 (HMGB1), phosphatidylserine (PS) and lysophosphatidic acid.
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RAGE activation further drives ROS production.
“and RAGE activation further drives ROS production,325”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [325]
GWAS found mutations within RAGE suggested to increase its affinity to ligands and enhance inflammatory response after activation by its ligand.
“Moreover, GWAS found mutations within RAGE which was suggested to increase its affinity to ligands and enhance inflammatory response after activated by its ligand.325”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [325]
RAGE-DIAPH1 interaction increases production of ROS and inflammatory cytokines, promotes cellular migration, and inhibits expression of cholesterol transporters, resulting in lipid accumulation and cellular dysfunction.
“RAGE-DIAPH1 interaction increases the production of ROS and inflammatory cytokines, promotes cellular migration, and inhibits the expression of cholesterol transporters (e.g., ABCA1, ABCG1), thereby resulting in lipid accumulation and cellular dysfunction.325”
From Role of neuroinflammation in neurodegeneration development (2023) · cites this paper as [325]
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Cited by
Sorted by citations
Role of neuroinflammation in neurodegeneration development
Zhang, W., Xiao, D., Mao, Q., & Xia, H. (2023) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-023-01486-5 · Cited by 1,668 · see citing works
“Moreover, GWAS found mutations within RAGE which was suggested to increase its affinity to ligands and enhance inflammatory response after activated by its ligand.(325) Aβ aggregates can act as DAMPs and induce RAGE-dependent inflammation signaling.”
Background
- Authors
- Derk, J., MacLean, M., Juranek, J., & Schmidt, A. M.
- Affiliations
- NYU Langone Health (US)
- Corresponding author
- Schmidt, Ann Marie
- Venue
- Journal of Alzheimer’s Disease & Parkinsonism
- Publisher
- OMICS Publishing Group
- Published
- 2018
- Volume
- 08
- Issue
- 01
- ISSN
- 2161-0460 (ISSN-L)
- PMC
- PMC6293973
- OpenAlex
- W2793481244
- Cited by
- 96
- References
- 19
- Citations by year
- 2026: 11 · 2025: 19 · 2024: 10 · 2023: 7 · 2022: 12 · 2021: 22 · 2020: 8 · 2019: 7
- FWCI
- 7.19
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by
- Locations
- Journal of Alzheimer’s Disease & Parkinsonism (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (F31AG054129)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- receptor for advanced glycation end products, RAGE, advanced glycation end products, neuroinflammation, neurodegeneration, amyloid-beta oligomers, high mobility group box 1, phosphatidylserine, lysophosphatidic acid, endothelial cells, microglia, astrocytes, Alzheimer's disease, Parkinson's disease
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