Role and Therapeutic Potential of RAGE Signaling in Neurodegeneration.
Advanced glycation end products receptor
Alzheimer’s disease
amyotrophic lateral sclerosis
astrocytes
microglia
neurons
parkinson’s disease
Journal
Current drug targets
ISSN: 1873-5592
Titre abrégé: Curr Drug Targets
Pays: United Arab Emirates
ID NLM: 100960531
Informations de publication
Date de publication:
2022
2022
Historique:
received:
28
02
2022
revised:
29
03
2022
accepted:
29
04
2022
pubmed:
16
6
2022
medline:
4
10
2022
entrez:
15
6
2022
Statut:
ppublish
Résumé
Activation of the receptor for advanced glycation end products (RAGE) has been shown to play an active role in the development of multiple neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and Amyotrophic Lateral Sclerosis. Although originally identified as a receptor for advanced glycation end products, RAGE is a pattern recognition receptor able to bind multiple ligands. The final outcome of RAGE signaling is defined in a context and cell type specific manner and can exert both neurotoxic and neuroprotective functions. Contributing to the complexity of the RAGE signaling network, different RAGE isoforms with distinctive signaling capabilities have been described. Moreover, multiple RAGE ligands bind other receptors and RAGE antagonism can significantly affect their signaling. Here, we discuss the outcome of celltype specific RAGE signaling in neurodegenerative pathologies. In addition, we will review the different approaches that have been developed to target RAGE signaling and their therapeutic potential. A clear understanding of the outcome of RAGE signaling in a cell type- and disease-specific manner would contribute to advancing the development of new therapies targeting RAGE. The ability to counteract RAGE neurotoxic signaling while preserving its neuroprotective effects would be critical for the success of novel therapies targeting RAGE signaling.
Identifiants
pubmed: 35702767
pii: CDT-EPUB-124378
doi: 10.2174/1389450123666220610171005
pmc: PMC9589927
mid: NIHMS1841674
doi:
Substances chimiques
Glycation End Products, Advanced
0
Ligands
0
Neuroprotective Agents
0
Protein Isoforms
0
Receptor for Advanced Glycation End Products
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, U.S. Gov't, Non-P.H.S.
Langues
eng
Sous-ensembles de citation
IM
Pagination
1191-1209Subventions
Organisme : NINDS NIH HHS
ID : R01 NS100835
Pays : United States
Informations de copyright
Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.
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