Membrane Cholesterol Interactions with Proteins in Hypercholesterolemia-Induced Endothelial Dysfunction.
Atherosclerosis
Cholesterol
Dyslipidemia
Endothelial dysfunction
Hypercholesterolemia
Kir2.1
Journal
Current atherosclerosis reports
ISSN: 1534-6242
Titre abrégé: Curr Atheroscler Rep
Pays: United States
ID NLM: 100897685
Informations de publication
Date de publication:
09 2023
09 2023
Historique:
accepted:
23
06
2023
medline:
1
9
2023
pubmed:
7
7
2023
entrez:
7
7
2023
Statut:
ppublish
Résumé
The goal of this review is to highlight work identifying mechanisms driving hypercholesterolemia-mediated endothelial dysfunction. We specifically focus on cholesterol-protein interactions and address specific questions related to the impact of hypercholesterolemia on cellular cholesterol and vascular endothelial function. We describe key approaches used to determine the effects of cholesterol-protein interactions in mediating endothelial dysfunction under dyslipidemic conditions. The benefits of removing the cholesterol surplus on endothelial function in models of hypercholesterolemia is clear. However, specific mechanisms driving cholesterol-induced endothelial dysfunction need to be determined. In this review, we detail the latest findings describing cholesterol-mediated endothelial dysfunction, highlighting our studies indicating that cholesterol suppresses endothelial Kir2.1 channels as a major underlying mechanism. The findings detailed in this review support the targeting of cholesterol-induced suppression of proteins in restoring endothelial function in dyslipidemic conditions. The identification of similar mechanisms regarding other cholesterol-endothelial protein interactions is warranted.
Identifiants
pubmed: 37418067
doi: 10.1007/s11883-023-01127-w
pii: 10.1007/s11883-023-01127-w
pmc: PMC10471518
doi:
Substances chimiques
Cholesterol
97C5T2UQ7J
Kir2.1 channel
0
Potassium Channels, Inwardly Rectifying
0
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
535-541Subventions
Organisme : NIGMS NIH HHS
ID : P20 GM113125
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL083298
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL141120
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL073965
Pays : United States
Informations de copyright
© 2023. The Author(s).
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