TMAO promotes vascular endothelial cell pyroptosis via the LPEAT-mitophagy pathway.
Biochem Biophys Res Commun
; 703: 149667, 2024 Apr 09.
Article
em En
| MEDLINE
| ID: mdl-38382362
ABSTRACT
Trimethylamine N-oxide (TMAO) is a novel risk factor for atherosclerosis, and its underlying regulatory mechanisms are under intensive investigation. Inflammation-related vascular endothelial damage is the major driver in atherogenic process. Pyroptosis, a type of proinflammatory programmed cell death, has been proved to promote the initiation and progression of atherosclerosis. In our study, we found that TMAO triggered endothelial cells excessive mitophagy, thereby facilitating pyroptosis. This process is mediated by the upexpression of phosphatidylethanolamine acyltransferase (LPEAT). These findings provide insights into TMAO-induced vascular endothelial cell damage and suggest that LPEAT may be a valuable target for the prevention and treatment of atherosclerosis.
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Texto completo:
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Base de dados:
MEDLINE
Assunto principal:
Células Endoteliais
/
Aterosclerose
Limite:
Humans
Idioma:
En
Revista:
Biochem Biophys Res Commun
Ano de publicação:
2024
Tipo de documento:
Article