Molecular basis of the therapeutic properties of hemorphins.
Cancer
Hemorphins
Insulin regulated aminopeptidase
Opioid receptor
Renin-angiotensin system
Journal
Pharmacological research
ISSN: 1096-1186
Titre abrégé: Pharmacol Res
Pays: Netherlands
ID NLM: 8907422
Informations de publication
Date de publication:
08 2020
08 2020
Historique:
received:
08
01
2020
revised:
09
04
2020
accepted:
20
04
2020
pubmed:
22
5
2020
medline:
5
6
2021
entrez:
22
5
2020
Statut:
ppublish
Résumé
Hemorphins are endogenous peptides, 4-10 amino acids long, belonging to the family of atypical opioid peptides released during the sequential cleavage of hemoglobin protein. Hemorphins have been shown to exhibit diverse therapeutic effects in both human and animal models. However, the precise cellular and molecular mechanisms involved in such effects remain elusive. In this review, we summarize and propose potential mechanisms based on studies that investigated the biological activity of hemorphins of different lengths on multiple therapeutic targets. Special emphasis is given to molecular events related to renin-angiotensin system (RAS), opioid receptors and insulin-regulated aminopeptidase receptor (IRAP). This review provides a comprehensive coverage of the molecular mechanisms that underpin the therapeutic potential of hemorphins. Furthermore, it highlights the role of various hemorphin residues in pathological conditions, which could be explored further for therapeutic purposes.
Identifiants
pubmed: 32438036
pii: S1043-6618(20)31163-4
doi: 10.1016/j.phrs.2020.104855
pii:
doi:
Substances chimiques
IL1RN protein, human
0
Interleukin 1 Receptor Antagonist Protein
0
Opioid Peptides
0
Receptors, Opioid
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
104855Informations de copyright
Copyright © 2020 Elsevier Ltd. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.