Mineralocorticoid Receptor Deficiency in Macrophages Inhibits Neointimal Hyperplasia and Suppresses Macrophage Inflammation Through SGK1-AP1/NF-κB Pathways
Author(s) -
Jianyong Sun,
Chao Li,
ZhuXia Shen,
WuChang Zhang,
Tang-Jun Ai,
LinJuan Du,
Yuyao Zhang,
Gao-Feng Yao,
Yan Liu,
Shuyang Sun,
Anikó NárayFejesTóth,
Géza FejesTóth,
Yong Peng,
Mao Chen,
Xiaojing Liu,
Jun Tao,
Bin Zhou,
Ying Yu,
Feifan Guo,
Jie Du,
ShengZhong Duan
Publication year - 2016
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.115.307031
Subject(s) - proinflammatory cytokine , neointimal hyperplasia , inflammation , vascular smooth muscle , endocrinology , medicine , macrophage , cancer research , restenosis , biology , biochemistry , smooth muscle , stent , in vitro
Restenosis after percutaneous coronary intervention remains to be a serious medical problem. Although mineralocorticoid receptor (MR) has been implicated as a potential target for treating restenosis, the cellular and molecular mechanisms are largely unknown. This study aims to explore the functions of macrophage MR in neointimal hyperplasia and to delineate the molecular mechanisms.
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