Insulin/IGF Axis and the Receptor for Advanced Glycation End Products: Role in Meta-inflammation and Potential in Cancer Therapy.
RAGE
cancer
diabetes
insulin/IGF system
meta-inflammation
obesity
Journal
Endocrine reviews
ISSN: 1945-7189
Titre abrégé: Endocr Rev
Pays: United States
ID NLM: 8006258
Informations de publication
Date de publication:
11 07 2023
11 07 2023
Historique:
received:
07
09
2022
medline:
13
7
2023
pubmed:
5
3
2023
entrez:
4
3
2023
Statut:
ppublish
Résumé
In metabolic conditions such as obesity and diabetes, which are associated with deregulated signaling of the insulin/insulin-like growth factor system (IIGFs), inflammation plays a dominant role. In cancer, IIGFs is implicated in disease progression, particularly during obesity and diabetes; however, further mediators may act in concert with IIGFs to trigger meta-inflammation. The receptor for advanced glycation end-products (RAGE) and its ligands bridge together metabolism and inflammation in obesity, diabetes, and cancer. Herein, we summarize the main mechanisms of meta-inflammation in malignancies associated with obesity and diabetes; we provide our readers with the most recent understanding and conceptual advances on the role of RAGE at the crossroad between impaired metabolism and inflammation, toward disease aggressiveness. We inform on the potential hubs of cross-communications driven by aberrant RAGE axis and dysfunctional IIGFs in the tumor microenvironment. Furthermore, we offer a rationalized view on the opportunity to terminate meta-inflammation via targeting RAGE pathway, and on the possibility to shut its molecular connections with IIGFs, toward a better control of diabetes- and obesity-associated cancers.
Identifiants
pubmed: 36869790
pii: 7069293
doi: 10.1210/endrev/bnad005
pmc: PMC10335176
doi:
Substances chimiques
Glycation End Products, Advanced
0
Insulin
0
Receptor for Advanced Glycation End Products
0
Somatomedins
0
AGER protein, human
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
693-723Informations de copyright
© The Author(s) 2023. Published by Oxford University Press on behalf of the Endocrine Society.
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