ArticleIranian journal of public health2021
Increased Mitochondrial DNA Copy Number and Oxidative Damage in Patients with Hashimoto's Thyroiditis.
Article in Iranian journal of public health, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- DNA Damage and Repair in Thyroid Physiology and Disease.Endocrine reviews · 2026Review
- Moderate NEFA reprogram early follicular development and oocyte competence: evidence for a targetable redox mechanism.Frontiers in nutrition · 2026Article
- Endoplasmic reticulum stress in Hashimoto's thyroiditis: a candidate amplification node linking thyroid-specific vulnerability and immune dysregulation.Frontiers in immunology · 2026Review
- Autoimmunity, New Potential Biomarkers and the Thyroid Gland-The Perspective of Hashimoto's Thyroiditis and Its Treatment.International journal of molecular sciences · 2024Review
- Association of Mitochondrial Variants with the Joint Occurrence of Polycystic Ovary Syndrome and Hashimoto's Thyroiditis.Antioxidants (Basel, Switzerland) · 2023Article
- Ozone Pollution, Oxidative Stress, Regulatory T Cells and Antioxidants.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe purpose of present study was to investigate mitochondrial DNA copy number (mtDNAcn) and mtDNA damage in peripheral blood of patients with Hashimoto's thyroiditis (HT) and healthy controls (HC).
methodsThe relative mtDNAcn and oxidative DNA damage in this case-control study were measured in peripheral blood of 50 patients with Hashimoto's thyroiditis and 50 healthy controls using quantitative real-time PCR. The study was conducted in Tehran University of Medical Sciences hospital, Tehran, Iran in 2018.
resultsHT patients had significantly higher mitochondrial DNA copy number and mitochondrial oxidative damage than the comparison group.
conclusionThese data suggest the possible involvement of mitochondria and oxidative stress in the pathophysiology of HT.
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Registered trials
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