Nrf2, a novel molecular target to reduce type 1 diabetes associated secondary complications: The basic considerations.
Antioxidant response element
Diabetes
Kelch-like ECH-associated protein 1 NADPH quinone dehydrogenase 1
Nuclear factor erythroid 2 (NFE2)-related factor 2
Reactive oxygen species
Journal
European journal of pharmacology
ISSN: 1879-0712
Titre abrégé: Eur J Pharmacol
Pays: Netherlands
ID NLM: 1254354
Informations de publication
Date de publication:
15 Jan 2019
15 Jan 2019
Historique:
received:
30
01
2018
revised:
10
10
2018
accepted:
17
10
2018
pubmed:
26
10
2018
medline:
16
4
2019
entrez:
26
10
2018
Statut:
ppublish
Résumé
Oxidative stress and inflammation are the mediators of diabetes and related secondary complications. Oxidative stress arises because of the excessive production of reactive oxygen species and diminished antioxidant production due to impaired Nrf2 activation, the master regulator of endogenous antioxidant. It has been established from various animal models that the transcription factor Nrf2 provides cytoprotection, ameliorates oxidative stress, inflammation and delays the progression of diabetes and its associated complications. Whereas, deletion of the transcription factor Nrf2 amplifies tissue level pathogenic alterations. In addition, Nrf2 also regulates the expression of numerous cellular defensive genes and protects against oxidative stress-mediated injuries in diabetes. The present review provides an overview on the role of Nrf2 in type 1 diabetes and explores if it could be a potential target for the treatment of diabetes and related complications. Further, the rationality of different agent's intervention has been discussed to mitigate organ damages induced by diabetes.
Identifiants
pubmed: 30359563
pii: S0014-2999(18)30611-3
doi: 10.1016/j.ejphar.2018.10.026
pii:
doi:
Substances chimiques
NF-E2-Related Factor 2
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
12-26Informations de copyright
Copyright © 2018. Published by Elsevier B.V.