Pathophysiological roles of NADPH oxidase/Nox family proteins in the vascular system review and perspective

Tetsuro Ago; Junya Kuroda; Masahiro Kamouchi; Junichi Sadoshima; Takanari Kitazono

doi:10.1253/circj.CJ-11-0388

Pathophysiological roles of NADPH oxidase/Nox family proteins in the vascular system review and perspective

Tetsuro Ago, Junya Kuroda, Masahiro Kamouchi, Junichi Sadoshima, Takanari Kitazono

研究成果: ジャーナルへの寄稿 › 評論記事

70 引用（Scopus）

抜粋

It has been established that oxidative stress plays a crucial role in the development and progression of vascular diseases. Besides the mitochondria, the NADPH oxidase/Nox family proteins are now thought to be important origins of the reactive oxygen species that underlie various vascular disease states, such as hypertension, atherosclerosis, angiogenesis, and ischemia/reperfusion injury. This review summarizes the basis of vascular Nox proteins and discusses their pathophysiological roles in the vascular system.

元の言語	英語
ページ（範囲）	1791-1800
ページ数	10
ジャーナル	Circulation Journal
巻	75
発行部数	8
DOI	https://doi.org/10.1253/circj.CJ-11-0388
出版物ステータス	出版済み - 8 1 2011

フィンガープリント

All Science Journal Classification (ASJC) codes

Cardiology and Cardiovascular Medicine

これを引用

Ago, T., Kuroda, J., Kamouchi, M., Sadoshima, J., & Kitazono, T. (2011). Pathophysiological roles of NADPH oxidase/Nox family proteins in the vascular system review and perspective. Circulation Journal, 75(8), 1791-1800. https://doi.org/10.1253/circj.CJ-11-0388

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AU - Kitazono, Takanari

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AB - It has been established that oxidative stress plays a crucial role in the development and progression of vascular diseases. Besides the mitochondria, the NADPH oxidase/Nox family proteins are now thought to be important origins of the reactive oxygen species that underlie various vascular disease states, such as hypertension, atherosclerosis, angiogenesis, and ischemia/reperfusion injury. This review summarizes the basis of vascular Nox proteins and discusses their pathophysiological roles in the vascular system.

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文献にアクセス

10.1253/circj.CJ-11-0388