ArticlePLoS genetics2017
Defective erythropoiesis caused by mutations of the thyroid hormone receptor α gene.
Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- Haematological Tracking of Thyroid Status During Methimazole Therapy and After Treatment Interruption in Hyperthyroid Cats: A Prospective Longitudinal Cohort Study.Veterinary sciences · 2026Article
- Prevalence and determinants of anemia in hypothyroidism and hyperthyroidism at the University of Gondar Comprehensive Specialized Hospital, Northwest Ethiopia.BMC endocrine disorders · 2026Article
- Bidirectional upregulation of Klotho by triiodothyronine and baicalein: mitigating chronic kidney disease and associated complications in aged BALB/c mice.Biogerontology · 2025Article
- TRα1 mutant suppresses KLF9 to cause endometrial metaplasia with ectopic IL-33 expression leading to uterine fibrosis and infertility.Scientific reports · 2025Article
- Article
- Hyperthyroidism-driven bone loss depends on BMP receptor Bmpr1a expression in osteoblasts.Communications biology · 2024Article
- Hematological Abnormalities and Associated Factors Among Patients with Hypothyroidism at the University of Gondar Comprehensive Specialized Hospital.Journal of blood medicine · 2024Article
- The plasma proteome reveals markers of recent and repeated stress in free-ranging seals.Conservation physiology · 2024Article
- Thyroid hormone receptor α1: a novel regulator of thyroid cancer cell differentiation.Oncogene · 2023Article
- Morphological and Functional Colonic Defects Caused by a Mutated Thyroid Hormone Receptor α.Thyroid : official journal of the American Thyroid Association · 2023Article
- Role of Nuclear Receptors in Controlling Erythropoiesis.International journal of molecular sciences · 2022Review
- Thyroid Function and Risk of Anemia: A Multivariable-Adjusted and Mendelian Randomization Analysis in the UK Biobank.The Journal of clinical endocrinology and metabolism · 2022Observational
- 3,3',5-Triiodothyroacetic acid (TRIAC) induces embryonic ζ-globin expression via thyroid hormone receptor α.Journal of hematology & oncology · 2021Article
- Thyroid Hormone Receptor α1 Mutants Impair B Lymphocyte Development in a Mouse Model.Thyroid : official journal of the American Thyroid Association · 2021Article
- Thyroid Hormone Receptor α Mutations Cause Heart Defects in Zebrafish.Thyroid : official journal of the American Thyroid Association · 2021Article
- Multiple mechanisms regulate H3 acetylation of enhancers in response to thyroid hormone.PLoS genetics · 2020Article
- Generation of Novel Genetic Models to Dissect Resistance to Thyroid Hormone Receptor α in Zebrafish.Thyroid : official journal of the American Thyroid Association · 2020Article
- Article
- Alteration in gene expression profile of thymomas with or without myasthenia gravis linked with the nuclear factor-kappaB/autoimmune regulator pathway to myasthenia gravis pathogenesis.Thoracic cancer · 2019Article
- Thyroid Hormone Receptor Alpha Mutations Lead to Epithelial Defects in the Adult Intestine in a Mouse Model of Resistance to Thyroid Hormone.Thyroid : official journal of the American Thyroid Association · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Patients with mutations of the THRA gene exhibit classical features of hypothyroidism, including erythroid disorders. We previously created a mutant mouse expressing a mutated TRα1 (denoted as PV; Thra1PV/+ mouse) that faithfully reproduces the classical hypothyroidism seen in patients. Using Thra1PV/+ mice, we explored how the TRα1PV mutant acted to cause abnormalities in erythropoiesis. Thra1PV/+ mice exhibited abnormal red blood cell indices similarly as reported for patients. The total bone marrow cells and erythrocytic progenitors were markedly reduced in the bone marrow of Thra1PV/+ mice. In vitro terminal differentiation assays showed a significant reduction of mature erythrocytes in Thra1PV/+ mice. In wild-type mice, the clonogenic potential of progenitors in the erythrocytic lineage was stimulated by thyroid hormone (T3), suggesting that T3 could directly accelerate the differentiation of progenitors to mature erythrocytes. Analysis of gene expression profiles showed that the key regulator of erythropoiesis, the Gata-1 gene, and its regulated genes, such as the Klf1, β-globin, dematin genes, CAII, band3 and eALAS genes, involved in the maturation of erythrocytes, was decreased in the bone marrow cells of Thra1PV/+ mice. We further elucidated that the Gata-1 gene was a T3-directly regulated gene and that TRα1PV could impair erythropoiesis via repression of the Gata-1 gene and its regulated genes. These results provide new insights into how TRα1 mutants acted to cause erythroid abnormalities in patients with mutations of the THRA gene. Importantly, the Thra1PV/+ mouse could serve as a preclinical mouse model to identify novel molecular targets for treatment of erythroid disorders.
Indexed as
Identifiers
What OpenQuestion holds
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.