ArticleProceedings of the National Academy of Sciences of the United States of America2014
Suppressing thyroid hormone signaling preserves cone photoreceptors in mouse models of retinal degeneration.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 67 citations in OpenAlex.
- The human THRB thyroid hormone receptor gene and the puzzle of retinal disease phenotypes.Developmental biology · 2026Review
- Photoreceptor deletion of pyruvate dehydrogenase E1 subunit α1 induces retinal degeneration and reprograms retinal metabolism.Molecular metabolism · 2026Article
- Article
- DIO3 coordinates photoreceptor development timing and fate stability in human retinal organoids.Genes & development · 2026Article
- The mechanisms, epidemiology, and clinical implications of thyroid hormones and age-related macular degeneration: a narrative review.Frontiers in medicine · 2026Review
- Dialogue Between the Clock Gene Bmal1 and Retinopathy: What Is the Exact Relationship?CNS neuroscience & therapeutics · 2025Review
- RIPK3 Contributes to Thyroid Hormone-Induced Photoreceptor Degeneration.International journal of molecular sciences · 2025Article
- Thyroid hormone signaling in ocular development and diseases.Biological research · 2025Review
- Differentiation versus dysfunction: thyroid hormone, deiodinases and retinal photoreceptors.European thyroid journal · 2025Review
- Resveratrol Protects Photoreceptors in Mouse Models of Retinal Degeneration.Antioxidants (Basel, Switzerland) · 2025Article
- Stimulation of Thyroid Hormone Signaling Induces Stress Responses in Mouse Retina.Advances in experimental medicine and biology · 2025Article
- Promotion of endoplasmic reticulum retrotranslocation by overexpression of E3 ubiquitin-protein ligase synoviolin 1 reduces endoplasmic reticulum stress and preserves cone photoreceptors in cyclic nucleotide-gated channel deficiency.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024Article
- Cone photoreceptor differentiation regulated by thyroid hormone transporter MCT8 in the retinal pigment epithelium.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Transcriptomic Analysis Reveals That Excessive Thyroid Hormone Signaling Impairs Phototransduction and Mitochondrial Bioenergetics and Induces Cellular Stress in Mouse Cone Photoreceptors.International journal of molecular sciences · 2024Article
- Thyroid Hormone Signaling in Retinal Development and Function: Implications for Diabetic Retinopathy and Age-Related Macular Degeneration.International journal of molecular sciences · 2024Review
- Immunogenetic and Environmental Factors in Age-Related Macular Disease.International journal of molecular sciences · 2024Review
- Risk Factors of Age-Related Macular Degeneration in a Population-Based Study: Results from SHIP-TREND-1 (Study of Health in Pomerania-TREND-1).Medical science monitor : international medical journal of experimental and clinical research · 2024Article
- Therapeutic potential of mackerel-derived peptides and the synthetic tetrapeptide TVGF for sleep disorders in a light-induced anxiety zebrafish model.Frontiers in pharmacology · 2024Article
- International Union of Basic and Clinical Pharmacology CXIII: Nuclear Receptor Superfamily-Update 2023.Pharmacological reviews · 2023Review
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Cone phototransduction and survival of cones in the human macula is essential for color vision and for visual acuity. Progressive cone degeneration in age-related macular degeneration, Stargardt disease, and recessive cone dystrophies is a major cause of blindness. Thyroid hormone (TH) signaling, which regulates cell proliferation, differentiation, and apoptosis, plays a central role in cone opsin expression and patterning in the retina. Here, we investigated whether TH signaling affects cone viability in inherited retinal degeneration mouse models. Retinol isomerase RPE65-deficient mice [a model of Leber congenital amaurosis (LCA) with rapid cone loss] and cone photoreceptor function loss type 1 mice (severe recessive achromatopsia) were used to determine whether suppressing TH signaling with antithyroid treatment reduces cone death. Further, cone cyclic nucleotide-gated channel B subunit-deficient mice (moderate achromatopsia) and guanylate cyclase 2e-deficient mice (LCA with slower cone loss) were used to determine whether triiodothyronine (T3) treatment (stimulating TH signaling) causes deterioration of cones. We found that cone density in retinol isomerase RPE65-deficient and cone photoreceptor function loss type 1 mice increased about sixfold following antithyroid treatment. Cone density in cone cyclic nucleotide-gated channel B subunit-deficient and guanylate cyclase 2e-deficient mice decreased about 40% following T3 treatment. The effect of TH signaling on cone viability appears to be independent of its regulation on cone opsin expression. This work demonstrates that suppressing TH signaling in retina dystrophy mouse models is protective of cones, providing insights into cone preservation and therapeutic interventions.
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