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  1. 学術雑誌論文
  2. 琉球医学会
  3. 琉球医学会誌
  4. 28巻3・4号
  1. 部局別インデックス
  2. その他

[総説]生体内における一酸化窒素合成酵素システムの意義の解明

http://hdl.handle.net/20.500.12000/0002016223
http://hdl.handle.net/20.500.12000/0002016223
49ea4848-7365-4e8e-b102-a628735408b0
名前 / ファイル ライセンス アクション
v28p7.pdf v28p7.pdf
Item type デフォルトアイテムタイプ(フル)(1)
公開日 2010-09-28
タイトル
タイトル [総説]生体内における一酸化窒素合成酵素システムの意義の解明
言語 ja
作成者 筒井, 正人

× 筒井, 正人

ja 筒井, 正人

Tsutsui, Masato

× Tsutsui, Masato

en Tsutsui, Masato

アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
権利情報
言語 ja
権利情報 琉球医学会
主題
言語 en
主題Scheme Other
主題 nitric oxide synthase
言語 en
主題Scheme Other
主題 knockout mouse
言語 en
主題Scheme Other
主題 cardiovascular disease
言語 en
主題Scheme Other
主題 myocardial infarction
言語 en
主題Scheme Other
主題 metabolic syndrome
内容記述
内容記述タイプ Other
内容記述 The nitric oxide (NO) synthases (NOSs) system consists of three different isoforms, including neuronal (nNOS), inducible (iNOS), and endothelial NOSs (eNOS). The roles of NO in vivo have been extensively investigated in pharmacological studies with NOS inhibitors. However, the NOS inhibitors possess multiple non-specific actions. Indeed, we clarified that vascular lesion formation caused by long-term treatment with the NOS inhibitors is not solely mediated by simple inhibition of vascular NO synthesis. Thus, the authentic roles of endogenous NO in our body still remain to be fully elucidated. To address this important issue, we have successfully developed mice in which all three NOS isoforms are completely disrupted. While the triply n/i/eNOS^<-/-> mice were unexpectedly viable and appeared normal, their survival and fertility rates were markedly reduced as compared with wild-type mice. Intriguingly, the triply n/i/eNOS^<-/-> mice, but not singly eNOS^<-/-> mice, spontaneously developed myocardial infarction accompanied by severe coronary arteriosclerotic lesions. Furthermore, the triply n/i/eNOS^<-/-> mice manifested abnormalities in a variety of systems, including the central nervous system, metabolic system, and bone system. These results provide the first evidence that genetic disruption of all three NOS genes causes a variety of disorders in mice in vivo, demonstrating a critical role of the endogenous NOS system in maintaining body homeostasis.
内容記述タイプ Other
内容記述 論文
出版者
言語 ja
出版者 琉球医学会
言語
言語 jpn
資源タイプ
資源タイプ journal article
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 1346-888X
収録物識別子タイプ ISSN
収録物識別子 0289-1530
収録物識別子タイプ NCID
収録物識別子 AN10369445
収録物名
言語 ja
収録物名 琉球医学会誌 = Ryukyu Medical Journal
書誌情報
巻 28, 号 3・4, p. 7-11
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