RAGE plays key role in diabetic retinopathy: a review.
AGE
Diabetic retinopathy
HMGB1
Inflammation
NF-κB
Neovascularization
RAGE
Treatment
Journal
Biomedical engineering online
ISSN: 1475-925X
Titre abrégé: Biomed Eng Online
Pays: England
ID NLM: 101147518
Informations de publication
Date de publication:
19 Dec 2023
19 Dec 2023
Historique:
received:
22
09
2023
accepted:
11
12
2023
medline:
20
12
2023
pubmed:
20
12
2023
entrez:
20
12
2023
Statut:
epublish
Résumé
RAGE is a multiligand receptor for the immunoglobulin superfamily of cell surface molecules and is expressed in Müller cells, vascular endothelial cells, nerve cells and RPE cells of the retina. Diabetic retinopathy (DR) is a multifactorial disease associated with retinal inflammation and vascular abnormalities and is the leading cause of vision loss or impairment in older or working-age adults worldwide. Therapies aimed at reducing the inflammatory response and unnecessary angiogenesis can help slow the progression of DR, which in turn can save patients' vision. To maximize the efficacy and minimize the side effects, treatments that target key players in the pathophysiological process of DR need to be developed. The interaction between RAGE and its ligands is involved in a variety of cytopathological alterations in the retina, including secretion of inflammatory factors, regulation of angiogenesis, oxidative stress, structural and functional changes, and neurodegeneration. In this review, we will summarize the pathologic pathways mediated by RAGE and its ligand interactions and discuss its role in the progression of diabetic retinopathy to explore potential therapeutic targets that are effective and safe for DR.
Identifiants
pubmed: 38115006
doi: 10.1186/s12938-023-01194-9
pii: 10.1186/s12938-023-01194-9
doi:
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
128Subventions
Organisme : The Science and Technology Project of Education Department of Jilin Province
ID : JJKH20190046KJ
Informations de copyright
© 2023. The Author(s).
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