Superoxide Dismutase 1 Loss Disturbs Intracellular Redox Signaling, Resulting in Global Age-Related Pathological Changes

Kenji Watanabe; Shuichi Shibuya; Yusuke Ozawa; Hidetoshi Nojiri; Naotaka Izuo; Koutaro Yokote; Takahiko Shimizu

doi:10.1155/2014/140165

Superoxide Dismutase 1 Loss Disturbs Intracellular Redox Signaling, Resulting in Global Age-Related Pathological Changes

Kenji Watanabe, Shuichi Shibuya, Yusuke Ozawa, Hidetoshi Nojiri, Naotaka Izuo, Koutaro Yokote, Takahiko Shimizu^*

^*この論文の責任著者

薬物治療学研究室

研究成果: ジャーナルへの寄稿 › 総説 › 査読

43 被引用数 (Scopus)

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Aging is characterized by increased oxidative stress, chronic inflammation, and organ dysfunction, which occur in a progressive and irreversible manner. Superoxide dismutase (SOD) serves as a major antioxidant and neutralizes superoxide radicals throughout the body. In vivo studies have demonstrated that copper/zinc superoxide dismutase-deficient (Sod1^-/-) mice show various aging-like pathologies, accompanied by augmentation of oxidative damage in organs. We found that antioxidant treatment significantly attenuated the age-related tissue changes and oxidative damage-associated p53 upregulation in Sod1^-/- mice. This review will focus on various age-related pathologies caused by the loss of Sod1 and will discuss the molecular mechanisms underlying the pathogenesis in Sod1^-/- mice.

本文言語	英語
論文番号	140165
ジャーナル	BioMed Research International
巻	2014
DOI	https://doi.org/10.1155/2014/140165
出版ステータス	出版済み - 2014

ASJC Scopus 主題領域

生化学、遺伝学、分子生物学一般
免疫学および微生物学一般

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10.1155/2014/140165

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title = "Superoxide Dismutase 1 Loss Disturbs Intracellular Redox Signaling, Resulting in Global Age-Related Pathological Changes",

abstract = "Aging is characterized by increased oxidative stress, chronic inflammation, and organ dysfunction, which occur in a progressive and irreversible manner. Superoxide dismutase (SOD) serves as a major antioxidant and neutralizes superoxide radicals throughout the body. In vivo studies have demonstrated that copper/zinc superoxide dismutase-deficient (Sod1-/-) mice show various aging-like pathologies, accompanied by augmentation of oxidative damage in organs. We found that antioxidant treatment significantly attenuated the age-related tissue changes and oxidative damage-associated p53 upregulation in Sod1-/- mice. This review will focus on various age-related pathologies caused by the loss of Sod1 and will discuss the molecular mechanisms underlying the pathogenesis in Sod1-/- mice.",

author = "Kenji Watanabe and Shuichi Shibuya and Yusuke Ozawa and Hidetoshi Nojiri and Naotaka Izuo and Koutaro Yokote and Takahiko Shimizu",

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doi = "10.1155/2014/140165",

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AU - Watanabe, Kenji

AU - Shibuya, Shuichi

AU - Ozawa, Yusuke

AU - Nojiri, Hidetoshi

AU - Izuo, Naotaka

AU - Yokote, Koutaro

AU - Shimizu, Takahiko

PY - 2014

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N2 - Aging is characterized by increased oxidative stress, chronic inflammation, and organ dysfunction, which occur in a progressive and irreversible manner. Superoxide dismutase (SOD) serves as a major antioxidant and neutralizes superoxide radicals throughout the body. In vivo studies have demonstrated that copper/zinc superoxide dismutase-deficient (Sod1-/-) mice show various aging-like pathologies, accompanied by augmentation of oxidative damage in organs. We found that antioxidant treatment significantly attenuated the age-related tissue changes and oxidative damage-associated p53 upregulation in Sod1-/- mice. This review will focus on various age-related pathologies caused by the loss of Sod1 and will discuss the molecular mechanisms underlying the pathogenesis in Sod1-/- mice.

AB - Aging is characterized by increased oxidative stress, chronic inflammation, and organ dysfunction, which occur in a progressive and irreversible manner. Superoxide dismutase (SOD) serves as a major antioxidant and neutralizes superoxide radicals throughout the body. In vivo studies have demonstrated that copper/zinc superoxide dismutase-deficient (Sod1-/-) mice show various aging-like pathologies, accompanied by augmentation of oxidative damage in organs. We found that antioxidant treatment significantly attenuated the age-related tissue changes and oxidative damage-associated p53 upregulation in Sod1-/- mice. This review will focus on various age-related pathologies caused by the loss of Sod1 and will discuss the molecular mechanisms underlying the pathogenesis in Sod1-/- mice.

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Superoxide Dismutase 1 Loss Disturbs Intracellular Redox Signaling, Resulting in Global Age-Related Pathological Changes

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