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.
authors.affiliation: 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.
authors.forename: Kenji
authors.identifier: 0000-0003-1707-1676
authors.initials: K
authors.lastname: Watanabe
authors.affiliation: Department of Advanced Aging Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
authors.forename: Shuichi
authors.identifier: 0000-0003-4050-0934
authors.initials: S
authors.lastname: Shibuya
authors.affiliation: Department of Advanced Aging Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
authors.forename: Yusuke
authors.identifier: 0000-0002-4660-6193
authors.initials: Y
authors.lastname: Ozawa
authors.affiliation: Department of Orthopaedics, Juntendo University Graduate School of Medicine, Bunkyo-ku, Tokyo 113-0033, Japan.
authors.forename: Hidetoshi
authors.identifier: 0000-0002-2359-3393
authors.initials: H
authors.lastname: Nojiri
authors.affiliation: Department of Advanced Aging Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
authors.forename: Naotaka
authors.identifier: 0000-0002-2642-5045
authors.initials: N
authors.lastname: Izuo
authors.affiliation: Department of Clinical Cell Biology and Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
authors.forename: Koutaro
authors.identifier: 0000-0003-3033-4813
authors.initials: K
authors.lastname: Yokote
authors.affiliation: Department of Advanced Aging Medicine, Chiba University Graduate School of Medicine, Chiba 260-8670, Japan.
authors.forename: Takahiko
authors.identifier: 0000-0002-3351-3342
authors.initials: T
authors.lastname: Shimizu
mesh_terms: D000375:Aging / Q000187:drug effects / Q000473:pathology*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D006801:Humans; D042541:Intracellular Space / Q000378:metabolism*; D010084:Oxidation-Reduction / Q000187:drug effects; D015398:Signal Transduction / Q000187:drug effects; D013482:Superoxide Dismutase / Q000172:deficiency / Q000378:metabolism*; D000072105:Superoxide Dismutase-1
chemical_list: D000975:Antioxidants; C000606290:SOD1 protein, human; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1