Deletion of the myeloid endothelin-B receptor confers long-term protection from angiotensin II-mediated kidney, eye and vessel injury.
endothelin
hypertension
macrophages
organ injury
Journal
Kidney international
ISSN: 1523-1755
Titre abrégé: Kidney Int
Pays: United States
ID NLM: 0323470
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
received:
19
03
2020
revised:
25
04
2020
accepted:
07
05
2020
pubmed:
23
6
2020
medline:
22
6
2021
entrez:
23
6
2020
Statut:
ppublish
Résumé
The endothelin system may be an important player in hypertensive end-organ injury as endothelin-1 increases blood pressure and is pro-inflammatory. The immune system is emerging as an important regulator of blood pressure and we have shown that the early hypertensive response to angiotensin-II infusion was amplified in mice deficient of myeloid endothelin-B (ET
Identifiants
pubmed: 32569653
pii: S0085-2538(20)30690-6
doi: 10.1016/j.kint.2020.05.042
pmc: PMC7652550
pii:
doi:
Substances chimiques
Endothelins
0
Receptor, Endothelin B
0
Angiotensin II
11128-99-7
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
1193-1209Subventions
Organisme : Medical Research Council
ID : MR/R017840/1
Pays : United Kingdom
Organisme : British Heart Foundation
ID : FS/13/30/29994
Pays : United Kingdom
Informations de copyright
Copyright © 2020 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.
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