Endothelial ACKR3 drives atherosclerosis by promoting immune cell adhesion to vascular endothelium.
ACKR3
Atherosclerosis
Endothelium
Inflammation
Vascular biology
Journal
Basic research in cardiology
ISSN: 1435-1803
Titre abrégé: Basic Res Cardiol
Pays: Germany
ID NLM: 0360342
Informations de publication
Date de publication:
08 06 2022
08 06 2022
Historique:
received:
13
10
2021
accepted:
12
05
2022
revised:
11
05
2022
entrez:
8
6
2022
pubmed:
9
6
2022
medline:
11
6
2022
Statut:
epublish
Résumé
Atherosclerosis is the foundation of potentially fatal cardiovascular diseases and it is characterized by plaque formation in large arteries. Current treatments aimed at reducing atherosclerotic risk factors still allow room for a large residual risk; therefore, novel therapeutic candidates targeting inflammation are needed. The endothelium is the starting point of vascular inflammation underlying atherosclerosis and we could previously demonstrate that the chemokine axis CXCL12-CXCR4 plays an important role in disease development. However, the role of ACKR3, the alternative and higher affinity receptor for CXCL12 remained to be elucidated. We studied the role of arterial ACKR3 in atherosclerosis using western diet-fed Apoe
Identifiants
pubmed: 35674847
doi: 10.1007/s00395-022-00937-4
pii: 10.1007/s00395-022-00937-4
pmc: PMC9177477
doi:
Substances chimiques
Cmkor1 protein, mouse
0
Receptors, CXCR
0
Rela protein, mouse
0
Transcription Factor RelA
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
30Informations de copyright
© 2022. The Author(s).
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