Open AccessAdenosine kinase is critical for neointima formation after vascular injury by inducing aberrant DNA hypermethylation
Author(s) -
Yong Wang,
Yiming Xu,
Siyuan Yan,
Kaixiang Cao,
Xiangwu Zeng,
Yaqi Zhou,
Zhiping Liu,
Qiuhua Yang,
Yue Pan,
Xiaoling Wang,
Detlev Boison,
Yunchao Su,
Xuejun Jiang,
Vijay Patel,
David Fulton,
Neal L. Weintraub,
Yuqing Huo
Publication year - 2020
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvaa040
Subject(s) - neointima , vascular smooth muscle , adenosine kinase , adenosine , klf4 , microbiology and biotechnology , dna methylation , cell growth , chemistry , cancer research , biology , medicine , biochemistry , endocrinology , gene expression , restenosis , adenosine deaminase , stent , gene , embryonic stem cell , smooth muscle , induced pluripotent stem cell
Adenosine receptors and extracellular adenosine have been demonstrated to modulate vascular smooth muscle cell (VSMC) proliferation and neointima formation. Adenosine kinase (ADK) is a major enzyme regulating intracellular adenosine levels but is function in VSMC remains unclear. Here, we investigated the role of ADK in vascular injury-induced smooth muscle proliferation and delineated the mechanisms underlying its action.