ArticlePloS one2009
Cytoprotective Nrf2 pathway is induced in chronically txnrd 1-deficient hepatocytes.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
What it found
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Who cites it
69 citing papers in PubMed, 116 citations in OpenAlex.
- Crosstalk Between Nrf2 and Metabolic Pathways: Redox Regulation, Glutaminolysis, and Cellular Proliferation.Cell biochemistry and biophysics · 2026Review
- Cystine C-S bond cleavage fuels cysteine production under disulfide reductase deficiency.Nature chemical biology · 2026Article
- Genome-Wide Association Study of Genetic Variants Associated with Serum Albumin Levels in Chinese Winter Sports Athletes.Biology · 2026Article
- Investigation of the effects of monosodium glutamate and tannic acid on the glutathione and thioredoxin systems in the liver of rats.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- NRF2 and Thioredoxin Reductase 1 as Modulators of Interactions between Zinc and Selenium.Antioxidants (Basel, Switzerland) · 2024Article
- Glutathione synthesis in the mouse liver supports lipid abundance through NRF2 repression.Nature communications · 2024Article
- Effects ofCancers · 2024Article
- Insights into the Multifaceted Roles of Thioredoxin-1 System: Exploring Knockout Murine Models.Biology · 2024Review
- Unresolved questions regarding cellular cysteine sources and their possible relationships to ferroptosis.Advances in cancer research · 2024Review
- Article
- Antioxidant Defense Capacity Is Reduced in Thyroid Stem/Precursor Cells Compared to Differentiated Thyrocytes.International journal of molecular sciences · 2023Article
- Short term starvation potentiates the efficacy of chemotherapy in triple negative breast cancer via metabolic reprogramming.Journal of translational medicine · 2023Article
- Neonatal Selenium Deficiency Decreases Selenoproteins in the Lung and Impairs Pulmonary Alveolar Development.Antioxidants (Basel, Switzerland) · 2022Article
- Deletion of Thioredoxin Reductase Disrupts Redox Homeostasis and Impairs β-Cell Function.Function (Oxford, England) · 2022Article
- The Potential Role of Curcumin in Modulating the Master Antioxidant Pathway in Diabetic Hypoxia-Induced Complications.Molecules (Basel, Switzerland) · 2021Review
- Supplemental Ascorbate Diminishes DNA Damage Yet Depletes Glutathione and Increases Acute Liver Failure in a Mouse Model of Hepatic Antioxidant System Disruption.Antioxidants (Basel, Switzerland) · 2021Article
- Effects of Mammalian Thioredoxin Reductase Inhibitors.Handbook of experimental pharmacology · 2021Article
- Carbonyl Reductase 1 Plays a Significant Role in Converting Doxorubicin to Cardiotoxic Doxorubicinol in Mouse Liver, but the Majority of the Doxorubicinol-Forming Activity Remains Unidentified.Drug metabolism and disposition: the biological fate of chemicals · 2020Article
- Article
- Genome-Wide CRISPR Screen Reveals Autophagy Disruption as the Convergence Mechanism That Regulates the NRF2 Transcription Factor.Molecular and cellular biology · 2019Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundMetabolically active cells require robust mechanisms to combat oxidative stress. The cytoplasmic thioredoxin reductase/thioredoxin (Txnrd1/Txn1) system maintains reduced protein dithiols and provides electrons to some cellular reductases, including peroxiredoxins. PRINCIPAL
findingsHere we generated mice in which the txnrd1 gene, encoding Txnrd1, was specifically disrupted in all parenchymal hepatocytes. Txnrd1-deficient livers exhibited a transcriptome response in which 56 mRNAs were induced and 12 were repressed. Based on the global hybridization profile, this represented only 0.3% of the liver transcriptome. Since most liver mRNAs were unaffected, compensatory responses were evidently effective. Nuclear pre-mRNA levels indicated the response was transcriptional. Twenty-one of the induced genes contained known antioxidant response elements (AREs), which are binding sites for the oxidative and chemical stress-induced transcription factor Nrf2. Txnrd1-deficient livers showed increased accumulation of nuclear Nrf2 protein and chromatin immunoprecipitation on the endogenous nqo1 and aox1 promoters in fibroblasts indicated that Txnrd1 ablation triggered in vivo assembly of Nrf2 on each.
conclusionsChronic deletion of Txnrd1 results in induction of the Nrf2 pathway, which contributes to an effective compensatory response.
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