ReviewEndocrine reviews2019
Paradigms of Dynamic Control of Thyroid Hormone Signaling.
Review in Endocrine reviews, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 papers, 2 of them syntheses that pooled it.
What it found
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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
150 citing papers in PubMed, 2 syntheses or guidelines pooled it, 281 citations in OpenAlex.
- Genetically predicted alterations in thyroid function are associated with the risk of benign prostatic disease.Frontiers in endocrinology · 2023Pooled it
- Association between thyroid function and Alzheimer's disease: A systematic review.Metabolic brain disease · 2021Pooled it
- Comparative Effectiveness of Levothyroxine, Desiccated Thyroid Extract, and Levothyroxine+Liothyronine in Hypothyroidism.The Journal of clinical endocrinology and metabolism · 2021Trial
- Higher Caloric Exposure in Critically Ill Patients Transiently Accelerates Thyroid Hormone Activation.The Journal of clinical endocrinology and metabolism · 2020Trial
- Trial
- Multiscale characterization and distribution of the thyroid hormone transporter MCT8 in the adult and aged human brain.Acta neuropathologica communications · 2026Article
- Review
- Targeting the Warburg Effect in Anaplastic Thyroid Carcinoma: Metabolic Vulnerabilities and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Review
- Type 2 deiodinase-dependent surge in thyroid hormone controls muscle stem cell quiescence and self-renewal.The Journal of clinical investigation · 2026Article
- Overnutrition in mice impairs thyroid hormone biosynthesis and utilization, causing hypothyroidism, despite remarkable thyroidal adaptations.The Journal of clinical investigation · 2026Article
- Longitudinal Changes in Thyroid Hormones and Serum Albumin Following CABG, AVR, and PCI: An Exploratory Electronic Medical Record Study.Medical sciences (Basel, Switzerland) · 2026Article
- Genetics of selenoproteins and selenoprotein metabolism - An overview of current concepts and emerging aspects.Redox biology · 2026Review
- The abnormal thyroxine signals triggers podocyte apoptosis in DN mice.In vitro cellular & developmental biology. Animal · 2026Article
- Thyrotoxicosis in MCT8 deficiency.The Journal of clinical endocrinology and metabolism · 2026Review
- Cortical thinning in subclinical hypothyroidism: structural and functional brain changes underlying cognitive impairment.BMC endocrine disorders · 2026Article
- Emerging Roles, Mechanisms, and Therapeutic Potential of Thyroid Hormones in Neurodegenerative Diseases: A Review.Brain sciences · 2026Review
- Iridophore apoptosis mediates socially-regulated developmental color pattern plasticity in an anemonefish.PLoS biology · 2026Article
- Detection of selection signatures in indigenous African cattle reveals genomic footprints of adaptation, production and temperament traits.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Significance of neuroendocrine systems and the gut-brain axis (GBA) in the regulation of obesity.PeerJ · 2026Review
90 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 3 countries.
Funding
Abstract
Thyroid hormone (TH) molecules enter cells via membrane transporters and, depending on the cell type, can be activated (i.e., T4 to T3 conversion) or inactivated (i.e., T3 to 3,3'-diiodo-l-thyronine or T4 to reverse T3 conversion). These reactions are catalyzed by the deiodinases. The biologically active hormone, T3, eventually binds to intracellular TH receptors (TRs), TRα and TRβ, and initiate TH signaling, that is, regulation of target genes and other metabolic pathways. At least three families of transmembrane transporters, MCT, OATP, and LAT, facilitate the entry of TH into cells, which follow the gradient of free hormone between the extracellular fluid and the cytoplasm. Inactivation or marked downregulation of TH transporters can dampen TH signaling. At the same time, dynamic modifications in the expression or activity of TRs and transcriptional coregulators can affect positively or negatively the intensity of TH signaling. However, the deiodinases are the element that provides greatest amplitude in dynamic control of TH signaling. Cells that express the activating deiodinase DIO2 can rapidly enhance TH signaling due to intracellular buildup of T3. In contrast, TH signaling is dampened in cells that express the inactivating deiodinase DIO3. This explains how THs can regulate pathways in development, metabolism, and growth, despite rather stable levels in the circulation. As a consequence, TH signaling is unique for each cell (tissue or organ), depending on circulating TH levels and on the exclusive blend of transporters, deiodinases, and TRs present in each cell. In this review we explore the key mechanisms underlying customization of TH signaling during development, in health and in disease states.
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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 Socratic graph.