Myocardial glucotoxicity: Mechanisms and potential therapeutic targets.
Adenosine monophosphate-activated protein kinase
Cardiomyopathie diabétique
Co-transporteurs aux sodium/glucose
Diabetes
Diabète
Glucotoxicity
Glucotoxicité
Heart failure
Insuffisance cardiaque
Protéine kinase activée par l’adénosine monophosphate
Sodium glucose cotransporter
Journal
Archives of cardiovascular diseases
ISSN: 1875-2128
Titre abrégé: Arch Cardiovasc Dis
Pays: Netherlands
ID NLM: 101465655
Informations de publication
Date de publication:
Nov 2020
Nov 2020
Historique:
received:
13
05
2020
revised:
01
06
2020
accepted:
03
06
2020
pubmed:
16
11
2020
medline:
16
12
2020
entrez:
15
11
2020
Statut:
ppublish
Résumé
Besides coronary artery disease, which remains the main cause of heart failure in patients with diabetes, factors independent of coronary artery disease are involved in the development of heart failure in the onset of what is called diabetic cardiomyopathy. Among them, hyperglycaemia - a hallmark of type 2 diabetes - has both acute and chronic deleterious effects on myocardial function, and clearly participates in the establishment of diabetic cardiomyopathy. In the present review, we summarize the cellular and tissular events that occur in a heart exposed to hyperglycaemia, and depict the complex molecular mechanisms proposed to be involved in glucotoxicity. Finally, from a more translational perspective, different therapeutic strategies targeting hyperglycaemia-mediated molecular mechanisms will be detailed.
Identifiants
pubmed: 33189592
pii: S1875-2136(20)30210-2
doi: 10.1016/j.acvd.2020.06.006
pii:
doi:
Substances chimiques
Blood Glucose
0
Hypoglycemic Agents
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
736-748Informations de copyright
Copyright © 2020 Elsevier Masson SAS. All rights reserved.