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α7 Nicotinic Acetylcholine Receptor Relieves Angiotensin II–Induced Senescence in Vascular Smooth Muscle Cells by Raising Nicotinamide Adenine Dinucleotide–Dependent SIRT1 Activity
Author(s) -
Dongjie Li,
Fang Huang,
Min Ni,
Hui Fu,
Liangsheng Zhang,
FuMing Shen
Publication year - 2016
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.116.307157
Subject(s) - angiotensin ii , downregulation and upregulation , nad+ kinase , sirtuin 1 , senescence , vascular smooth muscle , chemistry , nadph oxidase , nad(p)h oxidase , microbiology and biotechnology , nicotinamide adenine dinucleotide phosphate , signal transduction , nicotinamide phosphoribosyltransferase , reactive oxygen species , receptor , endocrinology , medicine , biology , oxidase test , biochemistry , enzyme , smooth muscle , gene
α7 nicotinic acetylcholine receptor (α7nAChR) is a subtype of nAChR and has been reported to be involved in hypertension end-organ damage. In this study, we tested the role of α7nAChR in angiotensin II (Ang II)-induced senescence of vascular smooth muscle cells (VSMCs).

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