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A Specific Role for eNOS-Derived Reactive Oxygen Species in Atherosclerosis Progression
Author(s) -
Tomofumi Takaya,
Ken–ichi Hirata,
Tomoya Yamashita,
Masakazu Shinohara,
Naoto Sasaki,
Nobutaka Inoue,
Toyotaka Yada,
Masami Goto,
Akiko Fukatsu,
Toshio Hayashi,
Nicholas J. C. King,
Keith M. Chan,
Mitsuhiro Yokoyama,
Seinosuke Kawashima
Publication year - 2007
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.107.142182
Subject(s) - reactive oxygen species , enos , medicine , cardiology , biology , chemistry , nitric oxide , biochemistry , nitric oxide synthase
When the availability of tetrahydrobiopterin (BH4) is deficient, endothelial nitric oxide synthase (eNOS) produces superoxide rather than NO (uncoupled eNOS). We have shown that the atherosclerotic lesion size was augmented in apolipoprotein E-deficient (ApoE-KO) mice overexpressing eNOS because of the enhanced superoxide production. In this study, we addressed the specific importance of uncoupled eNOS in atherosclerosis, and the potential mechanistic role for specific versus nonspecific antioxidant strategies in restoring eNOS coupling.

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