AgeR deletion decreases soluble fms-like tyrosine kinase 1 production and improves post-ischemic angiogenesis in uremic mice.
Animals
Biomarkers
/ blood
Cell Line
Gene Deletion
Humans
Ischemia
/ complications
Ligands
Male
Mice, Inbred C57BL
Neovascularization, Physiologic
RNA
/ metabolism
Receptor for Advanced Glycation End Products
/ deficiency
Solubility
Up-Regulation
Uremia
/ complications
Vascular Endothelial Growth Factor Receptor-1
/ biosynthesis
Angiogenesis
Chronic kidney disease
Ischemia–reperfusion
Receptor for advanced glycation end products
Soluble fms-like tyrosine kinase 1
Journal
Angiogenesis
ISSN: 1573-7209
Titre abrégé: Angiogenesis
Pays: Germany
ID NLM: 9814575
Informations de publication
Date de publication:
02 2021
02 2021
Historique:
received:
14
04
2020
accepted:
17
09
2020
pubmed:
30
9
2020
medline:
29
10
2021
entrez:
29
9
2020
Statut:
ppublish
Résumé
Peripheral arterial disease occurs more frequently and has a worse prognosis in patients with chronic kidney disease (CKD). The receptor for advanced glycation end products (RAGE) is involved in multiple aspects of uremia-associated vasculopathy. Previous data suggest that the RAGE pathway may promote soluble fms-like tyrosine kinase 1 (sFlt1) production, an anti-angiogenic molecule. Thus, we tested the hypothesis that the deletion of AgeR would decrease sFlt1 production and improve post-ischemic revascularization in uremic condition. We used a well-established CKD model (5/6 nephrectomy) in WT and AgeR
Identifiants
pubmed: 32989644
doi: 10.1007/s10456-020-09747-5
pii: 10.1007/s10456-020-09747-5
doi:
Substances chimiques
Biomarkers
0
Ligands
0
Receptor for Advanced Glycation End Products
0
RNA
63231-63-0
Vascular Endothelial Growth Factor Receptor-1
EC 2.7.10.1
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
47-55Références
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