1. Epigenetic Mechanisms in Vascular Inflammation: Modulation of Endothelial Adhesion Molecules and Endothelium-Leukocyte Adhesion.
- Author
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Calabriso N, Massaro M, Scoditti E, Carluccio C, Verri T, and Carluccio MA
- Subjects
- Humans, Intercellular Adhesion Molecule-1 genetics, Intercellular Adhesion Molecule-1 metabolism, Cell Adhesion genetics, Cell Adhesion Molecules genetics, Cell Adhesion Molecules metabolism, Endothelium metabolism, Leukocytes, Epigenesis, Genetic, Inflammation genetics, Inflammation metabolism, Endothelium, Vascular, Endothelial Cells metabolism, Vascular Cell Adhesion Molecule-1 genetics, Vascular Cell Adhesion Molecule-1 metabolism
- Abstract
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., Competing Interests: 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., (© 2023 The Author(s). Published by IMR Press.)
- Published
- 2023
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