ReviewEuropean thyroid journal2025
Differentiation versus dysfunction: thyroid hormone, deiodinases and retinal photoreceptors.
Review in European thyroid journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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Who cites it
4 citing papers in PubMed.
- The human THRB thyroid hormone receptor gene and the puzzle of retinal disease phenotypes.Developmental biology · 2026Review
- Single-Cell Sequencing Analysis Reveals Dysregulated Energy Metabolism and Altered Synaptic Connectivity in the Mouse Retina Following Dark Rearing.Investigative ophthalmology & visual science · 2026Article
- Thyroid hormone regulatory system in the mouse retina: integrated transcriptional and translational analysis of deiodinase enzymes, thyroid hormone receptors and thyroid hormone transporters.Cell communication and signaling : CCS · 2026Article
- Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
A growing body of evidence has established that thyroid hormone (triiodothyronine, T3) is a key factor in the differentiation and survival of the light-sensing photoreceptors in the retina. These functions include a critical role in generating the cone photoreceptor diversity that is required for color vision. Here, we review some of these functions of T3 and the critical mechanisms that regulate the T3 signal in the mammalian retina. The provision of T3, the active form of thyroid hormone, is determined by developmentally rising levels of T3 and its precursor T4 (thyroxine) in the circulation and by intrinsic control within the retina itself by deiodinase enzymes that deplete or amplify the available level of T3. Dynamic profiles of inactivating (DIO3) and activating (DIO2) deiodinases suggest that the T3 signal is progressively calibrated throughout early development, maturation and later functional maintenance of the retina. However, the benefits of T3 come at a cost: photoreceptors are susceptible to impairment and cell death when T3 signaling becomes imbalanced. These findings have implications regarding the influence of T3 in retinal diseases.
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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.