ReviewEuropean thyroid journal2013
Role of the NADPH Oxidases DUOX and NOX4 in Thyroid Oxidative Stress.
Review in European thyroid journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 77 citations in OpenAlex.
- Genotype-phenotype correlation of biallelic DUOX2 mutations in transient and permanent congenital hypothyroidism.Journal of the Endocrine Society · 2026Article
- Post-Chornobyl thyroid papillary carcinomas display distinct pastScientific reports · 2026Article
- Extracellular Vesicles, Nutrient Balance, and Redox Metabolism During Epididymal Sperm Maturation: A Perspective on the Complexity of Intercellular Interplay.Advances in anatomy, embryology, and cell biology · 2026Review
- Whole-genome sequencing GWAS reveals bovine genomic effects on enteric methane emissions in beef cattle.Scientific reports · 2025Article
- Investigation of the molecular mechanism of Xiaoluo Wan in thyroid-associated ophthalmopathy: network analysis and in vivo study.Hereditas · 2025Article
- NADPH oxidases: redox regulation of cell homeostasis and disease.Physiological reviews · 2025Review
- Status of Serum Levels of Oxidative Stress Biochemical Markers and Total Antioxidant Capacity in Primary Hypothyroidism.Reports of biochemistry & molecular biology · 2025Article
- Exploring the potential regulation of DUOX in thyroid hormone‑autophagy signaling via IGF‑1 in the skeletal muscle (Review).Biomedical reports · 2025Review
- Vitamin C in the Management of Thyroid Cancer: A Highway to New Treatment?Antioxidants (Basel, Switzerland) · 2024Review
- Redox Regulation by Priming Agents Toward a Sustainable Agriculture.Plant & cell physiology · 2024Review
- Involvement of Reactive Oxygen Species in Prostate Cancer and Its Disparity in African Descendants.International journal of molecular sciences · 2024Review
- Increased thyroid stimulating hormone (TSH) as a possible risk factor for atherosclerosis in subclinical hypothyroidism.Thyroid research · 2024Review
- Thyroid-associated ophthalmopathy: the role of oxidative stress.Frontiers in endocrinology · 2024Review
- Environmental Endocrinology: Parabens Hazardous Effects on Hypothalamic-Pituitary-Thyroid Axis.International journal of molecular sciences · 2023Review
- Gut microbiota short-chain fatty acids and their impact on the host thyroid function and diseases.Frontiers in endocrinology · 2023Review
- Review
- Population genetic differentiation and genomic signatures of adaptation to climate in an abundant lizard.Heredity · 2022Article
- NADPH Oxidase 4 (NOX4) in Cancer: Linking Redox Signals to Oncogenic Metabolic Adaptation.International journal of molecular sciences · 2022Review
- miR-199a Downregulation as a Driver of the NOX4/HIF-1α/VEGF-A Pathway in Thyroid and Orbital Adipose Tissues from Graves' Patients.International journal of molecular sciences · 2021Article
- Genetics of primary congenital hypothyroidism-a review.Hormones (Athens, Greece) · 2021Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatic mutations are present at high levels in the rat thyroid gland, indicating that the thyrocyte is under oxidative stress, a state in which cellular oxidant levels are high. The most important class of free radicals, or reactive metabolites, is reactive oxygen species (ROS), such as superoxide anion (O2 (-)), hydroxyl radical (OH) and hydrogen peroxide (H2O2). The main source of ROS in every cell type seems to be mitochondrial respiration; however, recent data support the idea that NADPH:O(2) oxidoreductase flavoproteins or simply NADPH oxidases (NOX) are enzymes specialized in controlled ROS generation at the subcellular level. Several decades ago, high concentrations of H2O2 were detected at the apical surface of thyrocytes, where thyroid hormone biosynthesis takes place. Only in the last decade has the enzymatic source of H2O2 involved in thyroid hormone biosynthesis been well characterized. The cloning of two thyroid genes encoding NADPH oxidases dual oxidases 1 and 2 (DUOX1 and DUOX2) revealed that DUOX2 mutations lead to hereditary hypothyroidism in humans. Recent reports have also described the presence of NOX4 in the thyroid gland and have suggested a pathophysiological role of this member of the NOX family. In the present review, we describe the participation of NADPH oxidases not only in thyroid physiology but also in gland pathophysiology, particularly the involvement of these enzymes in the regulation of thyroid oxidative stress.
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