Periostin induces kidney fibrosis after acute kidney injury via the p38 MAPK pathway.
Acute Kidney Injury
/ genetics
Animals
Cell Adhesion Molecules
/ genetics
Cell Line
Fibrosis
/ genetics
Humans
Kidney
/ blood supply
Male
Mice
Mice, Knockout
Phosphorylation
/ drug effects
Reperfusion Injury
/ genetics
Signal Transduction
/ drug effects
Transforming Growth Factor beta1
/ pharmacology
p38 Mitogen-Activated Protein Kinases
/ metabolism
fibrosis
hypoxia
p38 mitogen-activated protein kinase
periostin
unilateral ischemia-reperfusion injury
Journal
American journal of physiology. Renal physiology
ISSN: 1522-1466
Titre abrégé: Am J Physiol Renal Physiol
Pays: United States
ID NLM: 100901990
Informations de publication
Date de publication:
01 03 2019
01 03 2019
Historique:
pubmed:
13
12
2018
medline:
10
1
2020
entrez:
13
12
2018
Statut:
ppublish
Résumé
Periostin plays a crucial role in fibrosis, and acute kidney injury results in a high risk of progression to chronic kidney disease. Therefore, we hypothesized that periostin was involved in the progression of acute kidney injury to kidney fibrosis. Unilateral ischemia-reperfusion injury (UIRI) was induced in 7- to 8-wk-old male wild-type and periostin-null mice, and the animals were observed for 6 wk. In vitro, human kidney-2 cells and primary-cultured human tubular epithelial cells were incubated under hypoxic conditions (5% O
Identifiants
pubmed: 30539653
doi: 10.1152/ajprenal.00203.2018
doi:
Substances chimiques
Cell Adhesion Molecules
0
Postn protein, mouse
0
Transforming Growth Factor beta1
0
p38 Mitogen-Activated Protein Kinases
EC 2.7.11.24
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM