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Published on: June 18, 2020
Superoxide dismutase 1 loss disturbs intracellular redox signaling, resulting in global age-related pathological
Kenji Watanabe1, Shuichi Shibuya2, Yusuke Ozawa2
1Department 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.
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.
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