IL-6/Smad2 signaling mediates acute kidney injury and regeneration in a murine model of neonatal hyperoxia.
Acute Kidney Injury
/ metabolism
Animals
Animals, Newborn
Antioxidants
/ metabolism
Body Weight
Cell Proliferation
Disease Models, Animal
Female
Glomerular Filtration Rate
Hyperoxia
/ metabolism
Inflammation
Interleukin-6
/ genetics
Kidney Cortex
/ metabolism
Lung
/ metabolism
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Organ Size
Oxygen
/ metabolism
Regeneration
STAT3 Transcription Factor
/ metabolism
Smad2 Protein
/ metabolism
Transforming Growth Factor beta
/ metabolism
CKD
inflammation
neonatal chronic lung disease
nephrogenesis
Journal
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
ISSN: 1530-6860
Titre abrégé: FASEB J
Pays: United States
ID NLM: 8804484
Informations de publication
Date de publication:
05 2019
05 2019
Historique:
pubmed:
6
2
2019
medline:
2
6
2020
entrez:
6
2
2019
Statut:
ppublish
Résumé
Prematurity is linked to incomplete nephrogenesis and risk of chronic kidney diseases (CKDs). Oxygen is life-saving in that context but induces injury in numerous organs. Here, we studied the structural and functional impact of hyperoxia on renal injury and its IL-6 dependency. Newborn wild-type (WT) and IL-6 knockout (IL-6
Identifiants
pubmed: 30721632
doi: 10.1096/fj.201801875RR
doi:
Substances chimiques
Antioxidants
0
Interleukin-6
0
STAT3 Transcription Factor
0
Smad2 Protein
0
Smad2 protein, mouse
0
Stat3 protein, mouse
0
Transforming Growth Factor beta
0
interleukin-6, mouse
0
Oxygen
S88TT14065
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM