Highlights
- •HDACs regulate the progress of AS via modulating the limiting-enzymes activity involved in the metabolism of glucose and lipid.
- •HDACs effect the progress of AS through modulating the ECs activation and dysfunction.
- •HDACs modulate the macrophage derived foam cell and VSMC derived foam cell formation.
- •HDACs contribute to VSMCs phenotype switch and modulate the stability of plaque.
- •HDACs have an influence on the plaque disruption and thrombosis.
Abstract
Atherosclerosis is the most common pathological process that leads to cardiovascular
diseases, a disease of large- and medium-sized arteries that is characterized by a
formation of atherosclerotic plaques consisting of necrotic cores, calcified regions,
accumulated modified lipids, smooth muscle cells (SMCs), endothelial cells, leukocytes,
and foam cells. Recently, the question about how to suppress the occurrence of atherosclerosis
and alleviate the progress of cardiovascular disease becomes the hot topic. Accumulating
evidence suggests that histone deacetylases(HDACs) play crucial roles in arteriosclerosis.
This review summarizes the effect of HDACs and HDAC inhibitors(HDACi) on the progress
of atherosclerosis.
Keywords
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Article info
Publication history
Published online: December 23, 2014
Accepted:
December 18,
2014
Received in revised form:
December 17,
2014
Received:
July 10,
2014
Identification
Copyright
© 2015 Published by Elsevier Inc.
