ArticleFree radical biology & medicine2013
Dietary restriction attenuates the accelerated aging phenotype of Sod1(-/-) mice.
Article in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 40 citations in OpenAlex.
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- Mouse models used to test the role of reactive oxygen species in aging and age-related chronic diseases.Free radical biology & medicine · 2024Review
- Mapping the evolution of liver aging research: A bibliometric analysis.World journal of gastroenterology · 2024Article
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- Effect of Diet and Oxidative Stress in the Pathogenesis of Lymphoproliferative Disorders.Antioxidants (Basel, Switzerland) · 2023Review
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- Antioxidant Mitoquinone Alleviates Chronic Pancreatitis via Anti-Fibrotic and Antioxidant Effects.Journal of inflammation research · 2022Article
- Deletion of Neuronal CuZnSOD Accelerates Age-Associated Muscle Mitochondria and Calcium Handling Dysfunction That Is Independent of Denervation and Precedes Sarcopenia.International journal of molecular sciences · 2021Article
- Role of necroptosis in chronic hepatic inflammation and fibrosis in a mouse model of increased oxidative stress.Free radical biology & medicine · 2021Article
- Acute Kidney Injury is Aggravated in Aged Mice by the Exacerbation of Proinflammatory Processes.Frontiers in pharmacology · 2021Article
- The potential role of necroptosis in inflammaging and aging.GeroScience · 2019Review
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- Mouse Models of Accelerated Cellular Senescence.Methods in molecular biology (Clifton, N.J.) · 2019Article
- Restoration of SERCA ATPase prevents oxidative stress-related muscle atrophy and weakness.Redox biology · 2019Article
- Oxidative stress-induced dysregulation of excitation-contraction coupling contributes to muscle weakness.Journal of cachexia, sarcopenia and muscle · 2018Article
- Superoxide dismutases: Dual roles in controlling ROS damage and regulating ROS signaling.The Journal of cell biology · 2018Review
- SOD1 Phosphorylation by mTORC1 Couples Nutrient Sensing and Redox Regulation.Molecular cell · 2018Article
- The Geropathology Grading Platform demonstrates that mice null for Cu/Zn-superoxide dismutase show accelerated biological aging.GeroScience · 2018Article
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Dietary restriction is a powerful aging intervention that extends the life span of diverse biological species ranging from yeast to invertebrates to mammals, and it has been argued that the antiaging action of dietary restriction occurs through reduced oxidative stress/damage. Using Sod1(-/-) mice, which have previously been shown to have increased levels of oxidative stress associated with a shorter life span and a high incidence of neoplasia, we were able to test directly the ability of dietary restriction to reverse an aging phenotype due to increased oxidative stress/damage. We found that dietary restriction increased the life span of Sod1(-/-) mice 30%, returning it to that of wild-type, control mice fed ad libitum. Oxidative damage in Sod1(-/-) mice was markedly reduced by dietary restriction, as indicated by a reduction in liver and brain F2-isoprostanes, a marker of lipid peroxidation. Analysis of end of life pathology showed that dietary restriction significantly reduced the overall incidence of pathological lesions in the Sod1(-/-) mice fed the dietary-restricted diet compared to Sod1(-/-) mice fed ad libitum, including the incidence of lymphoma (27 vs 5%) and overall liver pathology. In addition to reduced incidence of overall and liver-specific pathology, the burden and severity of both neoplastic and nonneoplastic lesions was also significantly reduced in the Sod1(-/-) mice fed the dietary-restricted diet. These data demonstrate that dietary restriction can significantly attenuate the accelerated aging phenotype observed in Sod1(-/-) mice that arises from increased oxidative stress/damage.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.