ArticleThe Journal of cell biology2014
The thyroid hormone receptor β induces DNA damage and premature senescence.
Article in The Journal of cell biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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Who cites it
34 citing papers in PubMed, 66 citations in OpenAlex.
- Thyroid Hormone T3 Induces DNA Damage Response in Breast Cancer Cells.International journal of molecular sciences · 2026Article
- CellSNVReg: a multidimensional resource for SNV-mediated regulatory perturbations in single-cell and spatial omics.Nucleic acids research · 2026Article
- The circadian rhythm: A key variable in aging?Aging cell · 2024Article
- Causal linkage of Graves' disease with aging: Mendelian randomization analysis of telomere length and age-related phenotypes.BMC geriatrics · 2024Article
- Targeting Cell Senescence and Senolytics: Novel Interventions for Age-Related Endocrine Dysfunction.Endocrine reviews · 2024Review
- Targeting Androgen, Thyroid Hormone, and Vitamin A and D Receptors to Treat Prostate Cancer.International journal of molecular sciences · 2024Review
- Age-related variation in thyroid function - a narrative review highlighting important implications for research and clinical practice.Thyroid research · 2023Review
- Loss of p53 activates thyroid hormone via type 2 deiodinase and enhances DNA damage.Nature communications · 2023Article
- Article
- Aging under endocrine hormone regulation.Frontiers in endocrinology · 2023Review
- The thyroid hormone enhances mouse embryonic fibroblasts reprogramming to pluripotent stem cells: role of the nuclear receptor corepressor 1.Frontiers in endocrinology · 2023Article
- Article
- Thyroid receptor β might be responsible for breast cancer associated with Hashimoto's thyroiditis: a new insight into pathogenesis.Immunologic research · 2022Review
- Cross-Talk between the Cytokine IL-37 and Thyroid Hormones in Modulating Chronic Inflammation Associated with Target Organ Damage in Age-Related Metabolic and Vascular Conditions.International journal of molecular sciences · 2022Review
- Effects of Hypocalcemic Vitamin D Analogs in the Expression of DNA Damage Induced in Minilungs from hESCs: Implications for Lung Fibrosis.International journal of molecular sciences · 2022Article
- Regulation of metabolic and transcriptional responses by the thyroid hormone in cellular models of murine macrophages.Frontiers in immunology · 2022Article
- The Intriguing Thyroid Hormones-Lung Cancer Association as Exemplification of the Thyroid Hormones-Cancer Association: Three Decades of Evolving Research.International journal of molecular sciences · 2021Review
- Thyroid hormones in diabetes, cancer, and aging.Aging cell · 2020Review
- 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) and 8-hydroxy-2'-deoxyguanosine (8-OHdG) as a Cause of Autoimmune Thyroid Diseases (AITD) During Pregnancy?The Yale journal of biology and medicine · 2020Review
- Metabolic adaptations in spontaneously immortalized PGC-1α knock-out mouse embryonic fibroblasts increase their oncogenic potential.Redox biology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
There is increasing evidence that the thyroid hormone (TH) receptors (THRs) can play a role in aging, cancer and degenerative diseases. In this paper, we demonstrate that binding of TH T3 (triiodothyronine) to THRB induces senescence and deoxyribonucleic acid (DNA) damage in cultured cells and in tissues of young hyperthyroid mice. T3 induces a rapid activation of ATM (ataxia telangiectasia mutated)/PRKAA (adenosine monophosphate-activated protein kinase) signal transduction and recruitment of the NRF1 (nuclear respiratory factor 1) and THRB to the promoters of genes with a key role on mitochondrial respiration. Increased respiration leads to production of mitochondrial reactive oxygen species, which in turn causes oxidative stress and DNA double-strand breaks and triggers a DNA damage response that ultimately leads to premature senescence of susceptible cells. Our findings provide a mechanism for integrating metabolic effects of THs with the tumor suppressor activity of THRB, the effect of thyroidal status on longevity, and the occurrence of tissue damage in hyperthyroidism.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.