The interleukin-1 receptor type-1 in disturbed flow-induced endothelial mesenchymal activation.
activation
atherogenic
disturbed flow
endothelial-to-mesenchymal
interleukin-1 receptor type-1
Journal
Frontiers in cardiovascular medicine
ISSN: 2297-055X
Titre abrégé: Front Cardiovasc Med
Pays: Switzerland
ID NLM: 101653388
Informations de publication
Date de publication:
2023
2023
Historique:
received:
20
03
2023
accepted:
03
07
2023
medline:
4
8
2023
pubmed:
4
8
2023
entrez:
4
8
2023
Statut:
epublish
Résumé
Atherosclerosis is a progressive disease that develops in areas of disturbed flow (d-flow). Progressive atherosclerosis is characterized by bulky plaques rich in mesenchymal cells and high-grade inflammation that can rupture leading to sudden cardiac death or acute myocardial infarction. In response to d-flow, endothelial cells acquire a mesenchymal phenotype through endothelial-to-mesenchymal transition (EndMT). However, the signaling intermediaries that link d-flow to EndMT are incompletely understood. In this study we found that in human atherosclerosis, cells expressing SNAI1 (Snail 1, EndMT transcription factor) were highly expressed within the endothelial cell (EC) layer and in the pre-necrotic areas in unstable lesions, whereas stable lesions did not show any SNAI1 positive cells, suggesting a role for EndMT in lesion instability. The interleukin-1 (IL-1), which signals through the type-I IL-1 receptor (IL-1R1), has been implicated in plaque instability and linked to EndMT formation Global inhibition of IL-1 signaling in atherosclerosis as a therapeutic target has recently been tested in the completed CANTOS trial, with promising results. However, the data on IL-1R1 signaling in different vascular cell-types are inconsistent. Herein, we show endothelial IL-1R1 as a novel mechanosensitive receptor that couples d-flow to IL-1 signaling in EndMT.
Identifiants
pubmed: 37539090
doi: 10.3389/fcvm.2023.1190460
pmc: PMC10394702
doi:
Types de publication
Journal Article
Langues
eng
Pagination
1190460Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM121307
Pays : United States
Informations de copyright
© 2023 Kidder, Pea, Cheng, Koppada, Visvanathan, Henderson, Thuzar, Yu and Alfaidi.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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