Epigenetic Mechanisms in Vascular Inflammation: Modulation of Endothelial Adhesion Molecules and Endothelium-Leukocyte Adhesion.
DNA methylation
E-selectin
ICAM-1
NF-
RNA methylation
VCAM-1
cell adhesion molecules
histone modifications
lncRNAs
miRNAs
Journal
Frontiers in bioscience (Landmark edition)
ISSN: 2768-6698
Titre abrégé: Front Biosci (Landmark Ed)
Pays: Singapore
ID NLM: 101612996
Informations de publication
Date de publication:
06 09 2023
06 09 2023
Historique:
received:
30
05
2023
revised:
12
07
2023
accepted:
24
07
2023
medline:
2
11
2023
pubmed:
5
10
2023
entrez:
5
10
2023
Statut:
ppublish
Résumé
The endothelium, an essential component of the vascular system, plays a critical role in the inflammatory response. Under pro-inflammatory stimuli, endothelial cells undergo activation and dysfunction, leading to the release of inflammatory mediators and upregulation of cell adhesion molecules. These changes facilitate the adhesion, rolling, and transmigration of leukocytes into the subendothelial space. Emerging evidence suggests that epigenetic mechanisms, including nucleic acid methylation, post-translational histone modifications, and non-coding RNA, contribute significantly to the regulation of vascular inflammation and expression of cell adhesion molecules. Understanding the epigenetic molecular signatures that govern these processes may provide new insights into the development of therapeutic strategies to combat vascular inflammation and associated diseases. This review aims to summarize the current knowledge on the epigenetic mechanisms involved in modulating the intricate processes underlying vascular inflammation, with a specific focus on the expression of endothelial adhesion molecules and endothelium-leukocyte adhesion.
Identifiants
pubmed: 37796707
pii: S2768-6701(23)00979-6
doi: 10.31083/j.fbl2809194
doi:
Substances chimiques
Vascular Cell Adhesion Molecule-1
0
Intercellular Adhesion Molecule-1
126547-89-5
Cell Adhesion Molecules
0
Types de publication
Journal Article
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
194Informations de copyright
© 2023 The Author(s). Published by IMR Press.
Déclaration de conflit d'intérêts
Given their roles as Guest Editors, Nadia Calabriso and Maria Annunziata Carluccio, had no involvement in the peer-review of this article and have no access to information regarding its peer-review. The authors declare no conflict of interest.