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Novel mechanism of angiotensin II-induced cardiac injury in hypertensive rats: The critical role of ASK1 and VEGF
http://hdl.handle.net/2298/25964
http://hdl.handle.net/2298/25964ad023665-c3de-4cd6-97d9-a8fdf957b799
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Hypertension+Res.Table+Figure.pdf (353.9 kB)
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Hypertension+Res.35.2.194-200.pdf (123.0 kB)
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Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2012-11-30 | |||||
タイトル | ||||||
タイトル | Novel mechanism of angiotensin II-induced cardiac injury in hypertensive rats: The critical role of ASK1 and VEGF | |||||
言語 | ||||||
言語 | eng | |||||
キーワード | ||||||
主題 | oxidative stress, endothelial apoptosis, ASK1, VEGF, heart failure | |||||
資源タイプ | ||||||
資源タイプ | journal article | |||||
著者 |
Nako, Hisato
× Nako, Hisato× 片岡, 恵一郎× Koibuchi, Nobutaka× Dong, Yi-Fei× Toyama, Kensuke× 山本, 英一郎× Yasuda, Osamu× Ichijo, Hidenori× 小川, 久雄× 光山, 勝慶 |
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別言語の著者 |
名幸, 久仁
× 名幸, 久仁× 片岡, 恵一郎× 鯉渕, 信孝× 董, 一飛× 外山, 研介× 山本, 英一郎× 安田, 修× 一條, 秀憲× 小川, 久雄× 光山, 勝慶 |
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内容記述 | ||||||
内容記述 | This study was undertaken to elucidate a novel mechanism underlying angiotensin II-induced cardiac injury, focusing on the role of oxidative stress and myocardial capillary density. Salt-loaded Dahl salt-sensitive hypertensive rats (DS rats), a useful model for hypertensive cardiac remodeling or heart failure, were orally given irbesartan (an AT1 receptor blocker), tempol (a superoxide dismutase mimetic) or hydralazine (a vasodilator). Irbesartan significantly ameliorated left ventricular ischemia and prevented the development of cardiac hypertrophy and fibrosis in DS rats. The benefits were associated with the attenuation of oxidative stress, normalization of myocardial capillary density and inhibition of capillary endothelial apoptosis. Moreover, DS rats with significant cardiac hypertrophy and fibrosis displayed decreased myocardial vascular endothelial growth factor (VEGF) expression and increased cardiac apoptosis signal-regulating kinase 1 (ASK1) activation. Treatment with irbesartan significantly reversed these phenotypes. Tempol treatment of DS rats mimicked all the above-mentioned effects of irbesartan, indicating the critical role of oxidative stress in cardiac injury. We also investigated the role of VEGF and ASK1 in oxidative stress-induced endothelial apoptosis by using cultured endothelial cells from wild-type and ASK1-deficient mice. Oxidative stress-induced ASK1 activation led to endothelial apoptosis, and VEGF treatment prevented oxidative stress-induced endothelial apoptosis by inhibiting ASK1 activation. We obtained the first evidence that oxidative stress-induced cardiac VEGF repression and ASK1 activation caused the enhancement of endothelial apoptosis and contributed to a decrease in myocardial capillary density. These effects resulted in angiotensin II-induced progression of cardiac injury. | |||||
書誌情報 |
Hypertension Research 巻 35, 号 2, p. 194-200, 発行年 2012-02 |
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ISSN | ||||||
収録物識別子 | 09169636 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
関連識別子 | 10.1038/hr.2011.175 | |||||
フォーマット | ||||||
内容記述 | application/pdf | |||||
フォーマット | ||||||
内容記述 | application/pdf | |||||
形態 | ||||||
123009 bytes | ||||||
形態 | ||||||
353929 bytes | ||||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
日本十進分類法 | ||||||
主題 | 493 | |||||
出版者 | ||||||
出版者 | Nature Publishing Group | |||||
資源タイプ | ||||||
内容記述 | 論文(Article) | |||||
資源タイプ・ローカル | ||||||
雑誌掲載論文 | ||||||
資源タイプ・NII | ||||||
Journal Article | ||||||
資源タイプ・DCMI | ||||||
text | ||||||
資源タイプ・ローカル表示コード | ||||||
01 | ||||||
URL | ||||||
内容記述 | http://www.nature.com/hr/journal/v35/n2/abs/hr2011175a.html |