ReviewEndocrinology2021
Thyroid Hormone Deiodinases: Dynamic Switches in Developmental Transitions.
Review in Endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 43 citations in OpenAlex.
- The human THRB thyroid hormone receptor gene and the puzzle of retinal disease phenotypes.Developmental biology · 2026Review
- Article
- Genetics of selenoproteins and selenoprotein metabolism - An overview of current concepts and emerging aspects.Redox biology · 2026Review
- T3 enhances neuronal activity in an induced pluripotent stem cell derived model of early human brain development.European thyroid journal · 2026Article
- Cellular expression domains of type 3 deiodinase in the meninges, choroid plexus, tanycytes and barrier tissues of the brain.Frontiers in endocrinology · 2026Article
- A Comprehensive Review of Selenium as a Key Regulator in Thyroid Health.Biological trace element research · 2025Review
- Thyroid hormone promotes fetal neurogenesis.JCI insight · 2025Article
- Thyroid hormone promotes fetal neurogenesis.JCI insight · 2025Article
- Exploring the Antioxidant Roles of Cysteine and Selenocysteine in Cellular Aging and Redox Regulation.Biomolecules · 2025Review
- Serotonergic and Chemosensory Brain Areas and Sensory Ganglia Expressing Type 3 Deiodinase Mapped With Dio3Cre drivers.Endocrinology · 2025Article
- Differentiation versus dysfunction: thyroid hormone, deiodinases and retinal photoreceptors.European thyroid journal · 2025Review
- Effect of a Low-Molecular-Weight Allosteric Agonist of the Thyroid-Stimulating Hormone Receptor on Basal and Thyroliberin-Stimulated Activity of Thyroid System in Diabetic Rats.International journal of molecular sciences · 2025Article
- Transgenerational epigenetic self-memory ofEpigenetics · 2024Article
- Thyroid Hormone Signaling in Retinal Development and Function: Implications for Diabetic Retinopathy and Age-Related Macular Degeneration.International journal of molecular sciences · 2024Review
- Mice lacking DIO3 exhibit sex-specific alterations in circadian patterns of corticosterone and gene expression in metabolic tissues.BMC molecular and cell biology · 2024Article
- Biosynthesis, Engineering, and Delivery of Selenoproteins.International journal of molecular sciences · 2023Review
- Localized T3 production modifies the transcriptome and promotes the hepatocyte-like lineage in iPSC-derived hepatic organoids.JCI insight · 2023Article
- Single-cell profiling reveals Müller glia coordinate retinal intercellular communication during light/dark adaptation via thyroid hormone signaling.Protein & cell · 2023Article
- Developmental thyroid hormone action on pro-opiomelanocortin-expressing cells programs hypothalamic BMPR1A depletion and brown fat activation.Journal of molecular cell biology · 2023Article
- Thyroid Hormone Metabolism: A Historical Perspective.Thyroid : official journal of the American Thyroid Association · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Thyroid hormones exert pleiotropic, essential actions in mammalian, including human, development. These actions depend on provision of thyroid hormones in the circulation but also to a remarkable extent on deiodinase enzymes in target tissues that amplify or deplete the local concentration of the primary active form of the hormone T3 (3,5,3'-triiodothyronine), the high affinity ligand for thyroid hormone receptors. Genetic analyses in mice have revealed key roles for activating (DIO2) and inactivating (DIO3) deiodinases in cell differentiation fates and tissue maturation, ultimately promoting neonatal viability, growth, fertility, brain development, and behavior, as well as metabolic, endocrine, and sensory functions. An emerging paradigm is how the opposing activities of DIO2 and DIO3 are coordinated, providing a dynamic switch that controls the developmental timing of a tissue response, often during neonatal and maturational transitions. A second paradigm is how cell to cell communication within a tissue determines the response to T3. Deiodinases in specific cell types, often strategically located near to blood vessels that convey thyroid hormones into the tissue, can regulate neighboring cell types, suggesting a paracrine-like layer of control of T3 action. We discuss deiodinases as switches for developmental transitions and their potential to influence tissue dysfunction in human thyroid 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.