ArticleMechanisms of ageing and development2016
Liver specific expression of Cu/ZnSOD extends the lifespan of Sod1 null mice.
Article in Mechanisms of ageing and development, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Development of a targeted BioPROTAC degrader selective for misfolded SOD1.Nature communications · 2025Article
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- Alginate Oligosaccharides Repair Liver Injury by Improving Anti-Inflammatory Capacity in a Busulfan-Induced Mouse Model.International journal of molecular sciences · 2023Article
- Expression Profile of Housekeeping Genes and Tissue-Specific Genes in Multiple Tissues of Pigs.Animals : an open access journal from MDPI · 2022Article
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- Aging: All roads lead to mitochondria.Seminars in cell & developmental biology · 2021Article
- DNA Homeostasis and Senescence: Lessons from the Naked Mole Rat.International journal of molecular sciences · 2021Review
- Role of necroptosis in chronic hepatic inflammation and fibrosis in a mouse model of increased oxidative stress.Free radical biology & medicine · 2021Article
- Mitonuclear genomics and aging.Human genetics · 2020Review
- N- and O-Acetylated 3-Iodothyronamines Have No Metabolic or Thermogenic Effects in Male Mice.European thyroid journal · 2020Article
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- Insulin-like growth factor receptor signaling regulates working memory, mitochondrial metabolism, and amyloid-β uptake in astrocytes.Molecular metabolism · 2018Article
- Article
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Authors and funding
9 authors at 6 institutions in 1 country.
Funding
Abstract
Genetic ablation of CuZn-superoxide dismutase (Sod1) in mice (Sod1(-/-) mice) leads to shortened lifespan with a dramatic increase in hepatocellular carcinoma and accelerated aging phenotypes, including early onset sarcopenia. To study the tissue specific effects of oxidative stress in the Sod1(-/-) mice, we generated mice that only express the human SOD1 gene specifically in the liver of Sod1(-/-) mice (Sod1(-/-)/hSOD1(alb) mice). Expression of hSOD1 in the liver of Sod1(-/-) mice improved liver function, reduced oxidative damage in liver, and partially restored the expression of several genes involved in tumorigenesis, which are abnormally expressed in the livers of the Sod1(-/-) mice. However, liver specific expression of hSOD1 did not prevent the loss of body weight and muscle mass and alterations in the structure of neuromuscular junctions. The expression of hSOD1 in the liver of Sod1(-/-) mice significantly improved the lifespan of Sod1(-/-) mice; however, the lifespan of the Sod1(-/-)/hSOD1(alb) mice was still significantly shorter than wild type mice.
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