• Biomed Res Int · Jan 2014

    Review

    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, and Takahiko Shimizu.
    • Department of Advanced Aging Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan ; Department of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
    • Biomed Res Int. 2014 Jan 1;2014:140165.

    AbstractAging 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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