Absence of the β1 subunit of AMP-activated protein kinase reduces myofibroblast infiltration of the kidneys in early diabetes.
AMP-Activated Protein Kinases
/ deficiency
Albuminuria
/ metabolism
Animals
Blood Glucose
/ metabolism
Creatinine
/ metabolism
Diabetes Mellitus, Experimental
/ metabolism
Diabetes Mellitus, Type 1
/ enzymology
Diabetic Nephropathies
/ metabolism
Kidney
/ metabolism
Male
Mice, Inbred C57BL
Mice, Knockout
Myofibroblasts
/ physiology
Phosphorylation
AMPK
diabetes
fibrosis
myofibroblast
Journal
International journal of experimental pathology
ISSN: 1365-2613
Titre abrégé: Int J Exp Pathol
Pays: England
ID NLM: 9014042
Informations de publication
Date de publication:
04 2019
04 2019
Historique:
received:
30
04
2018
revised:
21
02
2019
accepted:
24
02
2019
pubmed:
27
4
2019
medline:
14
8
2019
entrez:
27
4
2019
Statut:
ppublish
Résumé
Activation of the heterotrimeric energy-sensing kinase AMP-activated protein kinase (AMPK) has been reported to improve experimental diabetic kidney disease. We examined the effect of type 1 diabetes in wild-type (WT) mice and mice lacking the β1 subunit of AMPK (AMPK β1
Identifiants
pubmed: 31025787
doi: 10.1111/iep.12313
pmc: PMC6540654
doi:
Substances chimiques
Blood Glucose
0
Creatinine
AYI8EX34EU
AMP-Activated Protein Kinases
EC 2.7.11.31
Types de publication
Journal Article
Langues
eng
Pagination
114-122Informations de copyright
© 2019 The Authors. International Journal of Experimental Pathology © 2019 International Journal of Experimental Pathology.
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