Beta-arrestins in the context of cardiovascular diseases: Focusing on angiotensin II type 1 receptor (AT1R).
Angiotensin II Type 1 Receptor Blockers
/ therapeutic use
Angiotensin-Converting Enzyme 2
/ metabolism
COVID-19
/ pathology
Cardiovascular Diseases
/ pathology
Cell Line
HEK293 Cells
Humans
Oligopeptides
/ therapeutic use
Receptor, Angiotensin, Type 1
/ metabolism
Renin-Angiotensin System
/ physiology
Signal Transduction
/ physiology
beta-Arrestins
/ metabolism
AT1R
Biased-agonism
Cardiac hypertrophy
Hypertension
Ischemia/reperfusion injury
Myocardial infarction
Renin-angiotensin-aldosterone system
SARS-CoV-2 infection
beta-Arrestin signaling
Journal
Cellular signalling
ISSN: 1873-3913
Titre abrégé: Cell Signal
Pays: England
ID NLM: 8904683
Informations de publication
Date de publication:
04 2022
04 2022
Historique:
received:
30
10
2021
revised:
16
01
2022
accepted:
18
01
2022
pubmed:
26
1
2022
medline:
8
3
2022
entrez:
25
1
2022
Statut:
ppublish
Résumé
Cardiovascular diseases are the leading cause of death worldwide. The renin-angiotensin-aldosterone system is one of the major regulators of cardiovascular homeostasis and the angiotensin II type 1 receptor (AT1R) mediates the main deleterious effects resulting from the hyperactivation of this hormonal system. Beta-arrestins are multifunctional proteins that regulate the desensitization and internalization of G protein-coupled receptors. After the discovery of beta-arrestins, many efforts have been made towards characterizing and distinguishing this new signaling pathway for drug discovery. Here, we summarize recent advances that address the beta-arrestin signaling in the cardiovascular system, focusing on the activation of the AT1R.
Identifiants
pubmed: 35077849
pii: S0898-6568(22)00013-4
doi: 10.1016/j.cellsig.2022.110253
pii:
doi:
Substances chimiques
Angiotensin II Type 1 Receptor Blockers
0
Oligopeptides
0
Receptor, Angiotensin, Type 1
0
beta-Arrestins
0
ACE2 protein, human
EC 3.4.17.23
Angiotensin-Converting Enzyme 2
EC 3.4.17.23
Sar-Arg-Val-Tyr-Ile-His-Pro-Ala-OH
J1J4P3PQZD
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
110253Informations de copyright
Copyright © 2022 Elsevier Inc. All rights reserved.