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Sulfasalazine induces haem oxygenase-1 via ROS-dependent Nrf2 signalling, leading to control of neointimal hyperplasia
Author(s) -
JuYoung Kim,
HyunJai Cho,
Jung-Ju Sir,
Baek-Kyung Kim,
Jin Hur,
SeockWon Youn,
HanMo Yang,
Soo-In Jun,
Kyung Woo Park,
Seok-Jae Hwang,
YooWook Kwon,
HaeYoung Lee,
HyunJae Kang,
ByungHee Oh,
Young-Bae Park,
Hyo-Soo Kim
Publication year - 2009
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/cvp072
Subject(s) - neointimal hyperplasia , vascular smooth muscle , reactive oxygen species , cancer research , inflammation , pharmacology , medicine , neointima , chemistry , microbiology and biotechnology , biology , restenosis , smooth muscle , stent
Inflammation, and the subsequent proliferative activity of vascular smooth muscle cells (VSMCs), is one of the major pathophysiological mechanisms associated with neointimal hyperplasia following vascular injury. Although sulfasalazine (SSZ) has been used as an anti-inflammatory and immune-modulatory agent in various inflammatory diseases, its primary targets and therapeutic effects on vascular disease have not yet been determined. We investigated whether SSZ could suppress VSMC growth and prevent neointimal hyperplasia.

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