ArticleOncogene2005
CuZnSOD deficiency leads to persistent and widespread oxidative damage and hepatocarcinogenesis later in life.
Article in Oncogene, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 307 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
307 citing papers in PubMed, 1 synthesis or guideline pooled it, 662 citations in OpenAlex.
- Superoxide Dismutase Administration: A Review of Proposed Human Uses.Molecules (Basel, Switzerland) · 2021Pooled it
- An antisense oligonucleotide against SOD1 delivered intrathecally for patients with SOD1 familial amyotrophic lateral sclerosis: a phase 1, randomised, first-in-man study.The Lancet. Neurology · 2013Trial
- Mitochondrial dysfunction in urologic disease.Prostate cancer and prostatic diseases · 2026Review
- Decoupling metabolic defense: Mutational and recombinational chaos in Sod1-deficient cells.PLoS genetics · 2026Article
- Harnessing copper-iron crosstalk: A novel strategy to combat hepatocellular carcinoma.Medical oncology (Northwood, London, England) · 2026Review
- Role of Focal Adhesion Kinase and NRF2 Pathways in Gastrointestinal Wound Healing.International journal of molecular sciences · 2026Review
- Clarifying the molecular mechanisms underlying the lethal in vitro cellular effects and mild organismal phenotype of SOD1 loss.Scientific reports · 2026Article
- Review
- Nutritional Strategies and Aging: Current Evidence and Future Directions.Molecules (Basel, Switzerland) · 2026Review
- Tissue-specific changes in antioxidant defence during ageing: the effect of chronic cold exposure.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2026Article
- Copper homeostasis and organelle-dependent mechanisms in bone metabolism: implications for osteoporosis therapy.Frontiers in cell and developmental biology · 2026Review
- L-ascorbate prevents non-alcoholic steatohepatitis-based hepatocarcinogenesis in Sod1/Prdx4 double-knockout mice.Scientific reports · 2025Article
- Association of TP53 with Defective Long Chain 3-Hydroxy acyl-CoA Dehydrogenase Induced Non-Cirrhotic Hepatocellular Carcinoma.Cancers · 2025Article
- Targeting cuproptosis in liver cancer: Molecular mechanisms and therapeutic implications.Apoptosis : an international journal on programmed cell death · 2025Review
- The Pathophysiology of Alcohol-Associated Liver Disease: Focusing on Superoxide Dismutase 1 as a Therapeutic Target.Biology · 2025Review
- Nanoparticles induced cuproptosis to enhance antitumor immunotherapy.Journal of nanobiotechnology · 2025Review
- CD103Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Article
- Maternal malnutrition induces inflammatory pathways and oxidative stress in the dorsolateral prostate of male offspring rats.Biogerontology · 2025Article
- Redox Balance in Cancer in the Context of Tumor Prevention and Treatment.Biomedicines · 2025Review
247 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 1 country.
Funding
Abstract
Mice deficient in CuZn superoxide dismutase (CuZnSOD) showed no overt abnormalities during development and early adulthood, but had a reduced lifespan and increased incidence of neoplastic changes in the liver. Greater than 70% of Sod1-/- mice developed liver nodules that were either nodular hyperplasia or hepatocellular carcinoma (HCC). Cross-sectional studies with livers collected from Sod1-/- and age-matched +/+ controls revealed extensive oxidative damage in the cytoplasm and, to a lesser extent, in the nucleus and mitochondria from as early as 3 months of age. A marked reduction in cytosolic aconitase, increased levels of 8-oxo dG and F2-isoprostanes, and a moderate reduction in glutathione peroxidase activities and porin levels were observed in all age groups of Sod1-/- mice examined. There were also age-related reductions in Mn superoxide dismutase activities and carbonic anhydrase III. Parallel to the biochemical changes, there were progressive increases in the DNA repair enzyme APEX1, the cell cycle control proteins cyclin D1 and D3, and the hepatocyte growth factor receptor Met. Increased cell proliferation in the presence of persistent oxidative damage to macromolecules likely contributes to hepatocarcinogenesis later in life.
Indexed as
Identifiers
What OpenQuestion holds
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.