Open AccessNew Mechanism of Rosiglitazone to Reduce Neointimal Hyperplasia
Author(s) -
Choon-Soo Lee,
YooWook Kwon,
HanMo Yang,
Sung Hwan Kim,
Tae Youn Kim,
Jin Hur,
Kyung Woo Park,
Hyun-Jai Cho,
HyunJae Kang,
Young-Bae Park,
HyoSoo Kim
Publication year - 2009
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.108.176230
Subject(s) - rosiglitazone , neointimal hyperplasia , neointima , endocrinology , medicine , protein kinase b , matrix metalloproteinase , chemistry , vascular smooth muscle , pharmacology , apoptosis , cancer research , receptor , restenosis , biochemistry , stent , smooth muscle
Mechanism of neointimal hyperplasia after vascular injury includes activation of signaling pathways and matrix metalloproteinases (MMPs) that are involved in cell proliferation and migration. Rosiglitazone, a synthetic peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist, was reported to inhibit neointimal hyperplasia in diabetic animals and humans. But the underlying mechanism has not been clarified. In this study, we examined how rosiglitazone inhibited neointimal hyperplasia.
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