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Review
. 2020 Nov 12:8:581015.
doi: 10.3389/fcell.2020.581015. eCollection 2020.

Histone Deacetylases (HDACs) and Atherosclerosis: A Mechanistic and Pharmacological Review

Affiliations
Review

Histone Deacetylases (HDACs) and Atherosclerosis: A Mechanistic and Pharmacological Review

Xiaona Chen et al. Front Cell Dev Biol. .

Abstract

Atherosclerosis (AS), the most common underlying pathology for coronary artery disease, is a chronic inflammatory, proliferative disease in large- and medium-sized arteries. The vascular endothelium is important for maintaining vascular health. Endothelial dysfunction is a critical early event leading to AS, which is a major risk factor for stroke and myocardial infarction. Accumulating evidence has suggested the critical roles of histone deacetylases (HDACs) in regulating vascular cell homeostasis and AS. The purpose of this review is to present an updated view on the roles of HDACs (Class I, Class II, Class IV) and HDAC inhibitors in vascular dysfunction and AS. We also elaborate on the novel therapeutic targets and agents in atherosclerotic cardiovascular diseases.

Keywords: HDAC inhibitors; atherosclerosis; endothelial dysfunction; epigenetic; histone deacetylation; macrophage; smooth muscle cells.

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Figures

FIGURE 1
FIGURE 1
Classification and sublocation of HDACs.
FIGURE 2
FIGURE 2
The potential mechanism of HDACs in atherosclerosis.

References

    1. Abend A., Shkedi O., Fertouk M., Caspi L. H., Kehat I. (2017). Salt-inducible kinase induces cytoplasmic histone deacetylase 4 to promote vascular calcification. EMBO Rep. 18 1166–1185. 10.15252/embr.201643686 - DOI - PMC - PubMed
    1. Abouhish H., Thounaojam M. C., Jadeja R. N., Gutsaeva D. R., Powell F. L., Khriza M., et al. (2020). Inhibition of HDAC6 attenuates diabetes-induced retinal redox imbalance and microangiopathy. Antioxidants 9:599. 10.3390/antiox9070599 - DOI - PMC - PubMed
    1. Alam S., Li H., Margariti A., Martin D., Zampetaki A., Habi O., et al. (2011). Galectin-9 protein expression in endothelial cells is positively regulated by histone deacetylase 3. J. Biol. Chem. 286 44211–44217. 10.1074/jbc.M111.242289 - DOI - PMC - PubMed
    1. Ali L., Schnitzler J. G., Kroon J. (2018). Metabolism: the road to inflammation and atherosclerosis. Curr. Opin. Lipidol. 29 474–480. 10.1097/mol.0000000000000550 - DOI - PubMed
    1. Ali M. M., Mahmoud A. M., Le Master E., Levitan I., Phillips S. A. (2019). Role of matrix metalloproteinases and histone deacetylase in oxidative stress-induced degradation of the endothelial glycocalyx. Am. J. Physiol. Heart Circ. Physiol. 316 H647–H663. 10.1152/ajpheart.00090.2018 - DOI - PMC - PubMed