Dual blockade of protease-activated receptor 1 and 2 additively ameliorates diabetic kidney disease.
Albuminuria
/ genetics
Animals
Cell Line
Cell Proliferation
/ drug effects
Collagen Type IV
/ metabolism
Cytokines
/ metabolism
Diabetes Mellitus, Type 1
/ drug therapy
Diabetic Nephropathies
/ genetics
Disease Models, Animal
Drug Therapy, Combination
Endothelial Cells
/ drug effects
Fibrosis
Humans
Imines
/ pharmacology
Inflammation Mediators
/ metabolism
Kidney
/ drug effects
Mice, 129 Strain
Mice, Inbred C57BL
Mice, Knockout
Nitric Oxide Synthase Type III
/ deficiency
Oligopeptides
/ pharmacology
Pyridines
/ pharmacology
Receptor, PAR-1
/ antagonists & inhibitors
Receptor, PAR-2
/ antagonists & inhibitors
Signal Transduction
coagulation
cytokine
endothelium
fibrosis
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 05 2020
01 05 2020
Historique:
pubmed:
24
3
2020
medline:
15
7
2020
entrez:
24
3
2020
Statut:
ppublish
Résumé
Protease-activated receptors (PARs) are coagulation protease targets, and they increase expression of inflammatory cytokines and chemokines in various diseases. Of all PARs, previous reports have shown that PAR1 or PAR2 inhibition is protective against diabetic glomerular injury. However, how PAR1 and PAR2 cooperatively contribute to diabetic kidney disease (DKD) pathogenesis and whether dual blockade of PARs is more effective in DKD remain elusive. To address this issue, male type I diabetic Akita mice heterozygous for endothelial nitric oxide synthase were used as a model of DKD. Mice (4 mo old) were divided into four treatment groups and administered vehicle, PAR1 antagonist (E5555, 60 mg·kg
Identifiants
pubmed: 32200667
doi: 10.1152/ajprenal.00595.2019
pmc: PMC7294339
doi:
Substances chimiques
Collagen Type IV
0
Cytokines
0
E 5555
0
F2RL1 protein, human
0
F2rl1 protein, mouse
0
H-Phe-Ser-Leu-Leu-Arg-Tyr-NH2
0
Imines
0
Inflammation Mediators
0
Oligopeptides
0
Pyridines
0
Receptor, PAR-1
0
Receptor, PAR-2
0
Nitric Oxide Synthase Type III
EC 1.14.13.39
Nos3 protein, mouse
EC 1.14.13.39
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
F1067-F1073Références
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