ArticlePloS one2013
Mitochondrial function in human neuroblastoma cells is up-regulated and protected by NQO1, a plasma membrane redox enzyme.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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
21 citing papers in PubMed, 40 citations in OpenAlex.
- Integrative multi-omics reveals NQO1-mediated airway epithelial injury as a key mechanism of bisphenol A-induced COPD.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Pharmacometabolomics uncovers key metabolic changes in the first-in-human study of β-lapachone derivative.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- NQO1 polymorphism and susceptibility to ischemic stroke in a Chinese population.BMC medical genomics · 2024Article
- A New Quinone-Based Inhibitor of Mitochondrial Complex I in D-Conformation, Producing Invasion Reduction and Sensitization to Venetoclax in Breast Cancer Cells.Antioxidants (Basel, Switzerland) · 2023Article
- NRF2: A crucial regulator for mitochondrial metabolic shift and prostate cancer progression.Frontiers in physiology · 2022Review
- A New Insight into an Alternative Therapeutic Approach to Restore Redox Homeostasis and Functional Mitochondria in Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2021Review
- Cooperation between CYB5R3 and NOX4 via coenzyme Q mitigates endothelial inflammation.Redox biology · 2021Article
- Increasing Nrf2 Activity as a Treatment Approach in Neuropsychiatry.Molecular neurobiology · 2021Review
- Docosahexanoic acid signals through the Nrf2-Nqo1 pathway to maintain redox balance and promote neurite outgrowth.Molecular biology of the cell · 2021Article
- Idebenone Ameliorates Rotenone-Induced Parkinson's Disease in Rats Through Decreasing Lipid Peroxidation.Neurochemical research · 2021Article
- Review
- Loss of NQO1 generates genotoxic estrogen-DNA adducts in Fuchs Endothelial Corneal Dystrophy.Free radical biology & medicine · 2020Article
- Mitohormesis in Mice via Sustained Basal Activation of Mitochondrial and Antioxidant Signaling.Cell metabolism · 2018Article
- Article
- Dihydroartemisinin inhibits the viability of cervical cancer cells by upregulating caveolin 1 and mitochondrial carrier homolog 2: Involvement of p53 activation and NAD(P)H:quinone oxidoreductase 1 downregulation.International journal of molecular medicine · 2017Article
- Novel high throughput pooled shRNA screening identifies NQO1 as a potential drug target for host directed therapy for tuberculosis.Scientific reports · 2016Article
- Calorie restriction as an intervention in ageing.The Journal of physiology · 2016Review
- Cytochrome b5 reductase, a plasma membrane redox enzyme, protects neuronal cells against metabolic and oxidative stress through maintaining redox state and bioenergetics.Age (Dordrecht, Netherlands) · 2015Article
- Differentiation of human neuroblastoma cells toward the osteogenic lineage by mTOR inhibitor.Cell death & disease · 2015Article
- Novel antioxidants protect mitochondria from the effects of oligomeric amyloid beta and contribute to the maintenance of epigenome function.ACS chemical neuroscience · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent findings suggest that NADH-dependent enzymes of the plasma membrane redox system (PMRS) play roles in the maintenance of cell bioenergetics and oxidative state. Neurons and tumor cells exhibit differential vulnerability to oxidative and metabolic stress, with important implications for the development of therapeutic interventions that promote either cell survival (neurons) or death (cancer cells). METHODS AND
findingsHere we used human neuroblastoma cells with low or high levels of the PMRS enzyme NADH-quinone oxidoreductase 1 (NQO1) to investigate how the PMRS modulates mitochondrial functions and cell survival. Cells with elevated NQO1 levels exhibited higher levels of oxygen consumption and ATP production, and lower production of reactive oxygen species. Cells overexpressing NQO1 were more resistant to being damaged by the mitochondrial toxins rotenone and antimycin A, and exhibited less oxidative/nitrative damage and less apoptotic cell death. Cells with basal levels of NQO1 resulted in increased oxidative damage to proteins and cellular vulnerability to mitochondrial toxins. Thus, mitochondrial functions are enhanced and oxidative stress is reduced as a result of elevated PMRS activity, enabling cells to maintain redox homeostasis under conditions of metabolic and energetic stress.
conclusionThese findings suggest that NQO1 is a potential target for the development of therapeutic agents for either preventing neuronal degeneration or promoting the death of neural tumor cells.
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.