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DNA methylation and histone post-translational modifications in atherosclerosis and a novel perspective for epigenetic therapy

Atherosclerosis, which is a vascular pathology characterized by inflammation and plaque build-up within arterial vessel walls, acts as the important cause of most cardiovascular diseases. Except for a lipid-depository and chronic inflammatory, increasing evidences propose that epigenetic modificatio...

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Detalles Bibliográficos
Autores principales: Zhang, Liang, Xia, Chenhai, Yang, Yongjun, Sun, Fangfang, Zhang, Yu, Wang, Huan, Liu, Rui, Yuan, Ming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10688481/
https://www.ncbi.nlm.nih.gov/pubmed/38031118
http://dx.doi.org/10.1186/s12964-023-01298-8
Descripción
Sumario:Atherosclerosis, which is a vascular pathology characterized by inflammation and plaque build-up within arterial vessel walls, acts as the important cause of most cardiovascular diseases. Except for a lipid-depository and chronic inflammatory, increasing evidences propose that epigenetic modifications are increasingly associated with atherosclerosis and are of interest from both therapeutic and biomarker perspectives. The chronic progressive nature of atherosclerosis has highlighted atherosclerosis heterogeneity and the fact that specific cell types in the complex milieu of the plaque are, by far, not the only initiators and drivers of atherosclerosis. Instead, the ubiquitous effects of cell type are tightly controlled and directed by the epigenetic signature, which, in turn, is affected by many proatherogenic stimuli, including low-density lipoprotein, proinflammatory, and physical forces of blood circulation. In this review, we summarize the role of DNA methylation and histone post-translational modifications in atherosclerosis. The future research directions and potential therapy for the management of atherosclerosis are also discussed. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12964-023-01298-8.