ArticleThe Journal of clinical endocrinology and metabolism2018
Stimulatory TSH-Receptor Antibodies and Oxidative Stress in Graves Disease.
Article in The Journal of clinical endocrinology and metabolism, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 51 citations in OpenAlex.
- Angiogenesis, Inflammation, and Oxidative Stress: Interrelationships in Autoimmune Thyroid Diseases.International journal of molecular sciences · 2026Article
- Ketogenic Diet and Thyroid Function: A Delicate Metabolic Balancing Act.Current issues in molecular biology · 2025Review
- Sex-Specific Cardiovascular Protection in Developing Metabolic Syndrome: The Role of AMPK.Antioxidants (Basel, Switzerland) · 2025Article
- [Level of reactive oxygen species production in peripheral blood monocytes in patients with Graves' disease after radioiodine therapy].Problemy endokrinologii · 2025Article
- Association between oxidative balance score and thyroid function and all-cause mortality in euthyroid adults.Scientific reports · 2025Article
- Increased thyroid stimulating hormone (TSH) as a possible risk factor for atherosclerosis in subclinical hypothyroidism.Thyroid research · 2024Review
- Association between thymic hyperplasia and serum calcium level in Graves' disease.BMC endocrine disorders · 2024Article
- Clinical significance of thyroglobulin antibodies and thyroid peroxidase antibodies in Graves' disease: a cross-sectional study.Hormones (Athens, Greece) · 2023Article
- Recent advances in graves ophthalmopathy medical therapy: a comprehensive literature review.International ophthalmology · 2023Review
- Thyrotropin Receptor Autoantibody Assessment in Thyroid Eye Disease: Does the Assay Type Matter?Korean journal of ophthalmology : KJO · 2023Article
- A Review of Testing for Distinguishing Hashimoto's Thyroiditis in the Hyperthyroid Stage and Grave's Disease.International journal of general medicine · 2023Review
- Male infertility and somatic health - insights into lipid damage as a mechanistic link.Nature reviews. Urology · 2022Review
- Brief Report - Monoclonal Antibodies Illustrate the Difficulties in Measuring Blocking TSH Receptor Antibodies.Frontiers in endocrinology · 2022Article
- The protective role of nutritional antioxidants against oxidative stress in thyroid disorders.Frontiers in endocrinology · 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
- The Influence of Oxidative Stress on Thyroid Diseases.Antioxidants (Basel, Switzerland) · 2021Article
- Thyrotropin receptor antibodies and Graves' orbitopathy.Journal of endocrinological investigation · 2021Review
- Type 1 Diabetes and Autoimmune Thyroid Disease-The Genetic Link.Frontiers in endocrinology · 2021Review
- A Novel Long-Term Graves' Disease Animal Model Confirmed by Functional Thyrotropin Receptor Antibodies.European thyroid journal · 2020Article
- Oxidative Stress in Graves Disease and Graves Orbitopathy.European thyroid journal · 2020Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Context: We hypothesized that TSH-receptor (TSHR) stimulating antibodies (TSAbs) are involved in oxidative stress mechanisms in patients with Graves disease (GD). Methods: Nicotinamide adenine dinucleotide phosphate oxidase, isoform 2 (NOX2); oxidative parameters; and oxidative burst were measured in serum, urine, and whole blood from patients with GD and control subjects. Superoxide production was investigated in human embryonic kidney (HEK)-293 cells stably overexpressing the TSHR. Lipid peroxidation was determined by immunodot-blot analysis for protein-bound 4-hydroxy-2-nonenal (4-HNE) in human primary thyrocytes and HEK-293-TSHR cells. Results: Serum NOX2 levels were markedly higher in hyperthyroid untreated vs euthyroid treated patients with GD, hyperthyroid patients with toxic nodular goiter, and euthyroid healthy control subjects (all P < 0.0001). Urine oxidative parameters were increased in patients with GD vs patients with toxic goiter (P < 0.01) and/or control subjects (P < 0.001). The maximum of the zymosan A- and phorbol 12,13-dibutyrate-induced respiratory burst of leukocytes was 1.5-fold higher in whole blood from hyperthyroid patients with GD compared with control subjects (P < 0.001 and P < 0.05). Monoclonal M22 TSAbs stimulated cAMP (HEK cells) in a dose-dependent manner. M22 (P = 0.0082), bovine TSH (P = 0.0028), and sera of hyperthyroid patients with GD (P < 0.05) increased superoxide-specific 2-hydroxyethidium levels in HEK-293 TSHR cells after 48-hour incubation vs control subjects. In contrast, triiodothyronine (T3) did not affect reactive oxygen species (ROS) production. In primary thyrocytes, the 4-HNE marker was higher in patients with GD vs control subjects at 6 and 48 hours (P = 0.02 and P = 0.04, respectively). Further, after 48-hour incubation of HEK-293 TSHR cells with patient sera, 4-HNE was higher in patients with untreated GD compared with control subjects (P < 0.05). Conclusions: Monoclonal M22 and polyclonal serum TSAbs augment ROS generation and/or induce lipid peroxidation.
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