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Epigenetic Regulation of Vascular Smooth Muscle Cell Proliferation and Neointima Formation by Histone Deacetylase Inhibition
Author(s) -
Hannes M. Findeisen,
Florence Gizard,
Yue Zhao,
Qing Hua,
Elizabeth B. Heywood,
Karrie L. Jones,
Dianne Cohn,
Dennis Bruemmer
Publication year - 2011
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.110.221952
Subject(s) - cyclin d1 , histone deacetylase , neointima , histone deacetylase 5 , microbiology and biotechnology , hdac11 , cancer research , biology , cyclin a , vascular smooth muscle , retinoblastoma protein , cell growth , hdac4 , histone deacetylase 2 , trichostatin a , cell cycle , histone , cell , biochemistry , medicine , endocrinology , gene , restenosis , smooth muscle , stent
Proliferation of smooth muscle cells (SMC) in response to vascular injury is central to neointimal vascular remodeling. There is accumulating evidence that histone acetylation constitutes a major epigenetic modification for the transcriptional control of proliferative gene expression; however, the physiological role of histone acetylation for proliferative vascular disease remains elusive.

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