Increased Mitochondrial DNA Copy Number and Oxidative Damage in Patients with Hashimoto’s Thyroiditis

Esfahanian, Fatemeh; Hazaveh, Mojgan Mirabdolhagh; Garehbagh, Laya Hooshmand; Falahati, Kowsar; Ataei, Mitra; Sanati, Mohammad Hossein; Jadali, Zohreh

doi:10.18502/ijph.v50i8.6817

Cited by 4 publications

(4 citation statements)

References 43 publications

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“…In the group of patients with subclinical hypothyroidism and HT, mean total oxidant status (TOS) and oxidative stress index (OSI) were significantly higher in individuals, who developed overt disorders, which raised the suspicion that oxidative stress may be an effective risk factor in the development of overt hypothyroidism in the course of HT [38]. According to already achieved data, mitochondrial DNA copy number (mtDNAcn) and mtDNA damage could be also perceived as other possible markers of OS in patients with HT [39,40]. It is worth mentioning here that microRNAs (miRNAs) are the small non-coding particles of RNA that regulate gene expression at the posttranscriptional level.…”

Section: Oxidative Stress In Thyroid Disordersmentioning

confidence: 99%

Autoimmunity, New Potential Biomarkers and the Thyroid Gland—The Perspective of Hashimoto’s Thyroiditis and Its Treatment

Tywanek,

Michalak,

Świrska

et al. 2024

IJMS

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Autoimmune thyroid disease (AITD) is the most common organic specific illness of the thyroid gland. It may manifest as the overproduction or the decline of thyroxine and triiodothyronine. Hyperthyroidism develops due to the overproduction of hormones as an answer to the presence of stimulatory antibodies against the TSH receptor. Hashimoto’s thyroiditis (HT) is generally characterized by the presence of thyroid peroxidase and thyroglobulin antibodies, with a concomitant infiltration of lymphocytes in the thyroid. Due to the progressive destruction of cells, AITD can lead to subclinical or overt hypothyroidism. Pathophysiology of AITD is extremely complicated and still not fully understood, with genetic, environmental and epigenetic factors involved in its development. Due to increasing incidence and social awareness of this pathology, there is an urgent need to expand the background concerning AITD. A growing body of evidence suggests possible ways of treatment apart from traditional approaches. Simultaneously, the role of potential new biomarkers in the diagnosis and monitoring of AITD has been highlighted recently, too. Therefore, we decided to review therapeutic trends in the course of AITD based on its pathophysiological mechanisms, mainly focusing on HT. Another aim was to summarize the state of knowledge regarding the role of new biomarkers in this condition.

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Section: Oxidative Stress In Thyroid Disordersmentioning

confidence: 99%

Autoimmunity, New Potential Biomarkers and the Thyroid Gland—The Perspective of Hashimoto’s Thyroiditis and Its Treatment

Tywanek,

Michalak,

Świrska

et al. 2024

IJMS

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“…The role of oxidative stress has been shown in many autoimmune diseases such as systemic sclerosis, myasthenia gravis, dermatomyositis, vitiligo, and Hashimoto’s thyroiditis, among others [ 30 , 31 , 32 , 33 , 34 ]. In a recent study, the levels of ROS in peripheral blood neutrophils of patients with rheumatoid arthritis (RA) were evaluated, which, in addition to being elevated, were associated with the severity of the disease [ 35 ].…”

Section: Regulatory T Cells and Diseasementioning

confidence: 99%

Ozone Pollution, Oxidative Stress, Regulatory T Cells and Antioxidants

et al. 2022

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Ozone pollution, is a serious health problem worldwide. Repeated exposure to low ozone doses causes a loss of regulation of the oxidation–reduction systems, and also induces a chronic state of oxidative stress. This fact is of special importance for the regulation of different systems including the immune system and the inflammatory response. In addition, the oxidation–reduction balance modulates the homeostasis of these and other complex systems such as metabolism, survival capacity, cell renewal, and brain repair, etc. Likewise, it has been widely demonstrated that in chronic degenerative diseases, an alteration in the oxide-reduction balance is present, and this alteration causes a chronic loss in the regulation of the immune response and the inflammatory process. This is because reactive oxygen species disrupt different signaling pathways. Such pathways are related to the role of regulatory T cells (Treg) in inflammation. This causes an increase in chronic deterioration in the degenerative disease over time. The objective of this review was to study the relationship between environmental ozone pollution, the chronic state of oxidative stress and its effect on Treg cells, which causes the loss of regulation in the inflammatory response as well as the role played by antioxidant systems in various pathologies.

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“…However, it should be noted that the majority of those studies were conducted in Asian populations. One study indicated significantly higher mitochondrial DNA CN and mitochondrial oxidative damage in HT patients [17]. To date, mtDNA variations have not been investigated in terms of PCOS and HT comorbidity.…”

Section: Introductionmentioning

confidence: 99%

Association of Mitochondrial Variants with the Joint Occurrence of Polycystic Ovary Syndrome and Hashimoto’s Thyroiditis

Zeber-Lubecka,

Kulecka,

Suchta

et al. 2023

Antioxidants

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Background. The prevalence of Hashimoto’s thyroiditis (HT) among women with polycystic ovary syndrome (PCOS) is higher than in the general female population, but the factors predisposing to the coexistence of these disorders remain unclear. This study employed whole genome sequencing of mitochondrial DNA to identify genetic variants potentially associated with the development of PCOS and HT and predisposing to their joint occurrence. Results. A total of 84 women participated, including patients with PCOS, HT, coexisting PCOS and HT (PCOS + HT) and healthy women. Both Fisher’s exact and Mann–Whitney U statistical analyses were performed to compare the frequency of variants between groups. Ten differentiating variants were common to both analyses in PCOS + HT vs. PCOS, one in PCOS + HT vs. HT, and six in PCOS + HT vs. control. Several variants differentiating the PCOS + HT group from PCOS and controls were identified, located both in the mitochondrial genes (including the MT-CYB, MT-ND1, MT-ND2, MT-ND4, MT-ND6, MT-CO1, MT-CO3) and the D-loop region. Only two variants differentiated PCOS + HT and HT groups. One variant (13237a in MT-ND5) was common for all three comparisons and underrepresented in the PCOS + HT group. Functional enrichment analysis showed 10 pathways that were unique for the comparison of PCOS + HT and PCOS groups, especially related to ATP production and oxidative phosphorylation, and one pathway, the NADH-quinone oxidoreductase, chain M/4, that was unique for the comparison of PCOS + HT and control groups. Notably, nine pathways shared commonality between PCOS + HT vs. PCOS and PCOS + HT vs. control, related to the biogenesis and assembly of Complex I. Conclusion. This study provides novel insights into the genetic variants associated with oxidative stress in women with coexisting PCOS and HT. Mitochondrial dysfunction and oxidative stress appear to play a role in the pathogenesis of both conditions. However, more mitochondrial variants were found to differentiate women with both PCOS and HT from those with PCOS alone than from those with HT alone.

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Increased Mitochondrial DNA Copy Number and Oxidative Damage in Patients with Hashimoto’s Thyroiditis

Cited by 4 publications

References 43 publications

Autoimmunity, New Potential Biomarkers and the Thyroid Gland—The Perspective of Hashimoto’s Thyroiditis and Its Treatment

Autoimmunity, New Potential Biomarkers and the Thyroid Gland—The Perspective of Hashimoto’s Thyroiditis and Its Treatment

Ozone Pollution, Oxidative Stress, Regulatory T Cells and Antioxidants

Association of Mitochondrial Variants with the Joint Occurrence of Polycystic Ovary Syndrome and Hashimoto’s Thyroiditis

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