ArticleCell metabolism2014
Intracellular inactivation of thyroid hormone is a survival mechanism for muscle stem cell proliferation and lineage progression.
Article in Cell metabolism, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
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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.
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Who cites it
72 citing papers in PubMed, 126 citations in OpenAlex.
- Type 2 deiodinase-dependent surge in thyroid hormone controls muscle stem cell quiescence and self-renewal.The Journal of clinical investigation · 2026Article
- Genetics of selenoproteins and selenoprotein metabolism - An overview of current concepts and emerging aspects.Redox biology · 2026Review
- Rhabdomyolysis in a patient with lung cancer with sintilimab-induced overlap syndrome and hypothyroidism: A case report.Experimental and therapeutic medicine · 2026Article
- Simultaneous improvement of breast muscle yield and meat quality in Langshan chickens.Poultry science · 2026Article
- Hypothyroidism impairs skeletal muscle regeneration after injury by altering myogenic and nonmyogenic pathways.JCI insight · 2026Article
- Transcriptome analysis of injured muscle identifies new candidate genes for satellite cell growth and myofiber formation during early muscle regeneration.Animal bioscience · 2026Article
- Beyond hormone deficiency: a framework for endocrine-immune-niche integration in aging skeletal muscle regeneration.Frontiers in immunology · 2026Review
- Endocrine control of skeletal muscle regeneration and clinical applications.Nature reviews. Endocrinology · 2026Article
- Functional role of THRAP3 in modulating thyroid hormone-mediated gene networks in C2C12 myotubes.PloS one · 2026Article
- Thyroid hormones and metabolic flexibility: tissue-specific control of energy homeostasis.Frontiers in physiology · 2026Review
- Genetic Deletion of the Purinergic ReceptorACS pharmacology & translational science · 2025Article
- Differentiation versus dysfunction: thyroid hormone, deiodinases and retinal photoreceptors.European thyroid journal · 2025Review
- Type 2 Deiodinase Promotes Fatty Adipogenesis in Muscle Fibroadipogenic Progenitors From Adult Male Mice.Endocrinology · 2025Article
- Type 3 deiodinase activation mediated by the Shh/Gli1 axis promotes sepsis-induced metabolic dysregulation in skeletal muscles.Burns & trauma · 2025Article
- The key roles of thyroid hormone in mitochondrial regulation, at interface of human health and disease.Journal of basic and clinical physiology and pharmacology · 2024Review
- Transcriptome profiling of longissimus dorsi during different prenatal stages to identify genes involved in intramuscular fat deposition in lean and obese pig breeds.Molecular biology reports · 2024Article
- Exploring the association between muscle mass and thyroid function in Chinese community subjects over 45 years old with normal thyroid function: a cross-sectional analysis.Frontiers in endocrinology · 2024Article
- Article
- DNA-PKcs regulates myogenesis in an Akt-dependent manner independent of induced DNA damage.Cell death and differentiation · 2023Article
- Deiodinases in thyroid tumorigenesis.Endocrine-related cancer · 2023Review
12 more citing papers are in PubMed but not listed here.
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Authors and funding
16 authors at 8 institutions in 3 countries.
Funding
Abstract
Precise control of the thyroid hormone (T3)-dependent transcriptional program is required by multiple cell systems, including muscle stem cells. Deciphering how this is achieved and how the T3 signal is controlled in stem cell niches is essentially unknown. We report that in response to proliferative stimuli such as acute skeletal muscle injury, type 3 deiodinase (D3), the thyroid hormone-inactivating enzyme, is induced in satellite cells where it reduces intracellular thyroid signaling. Satellite cell-specific genetic ablation of dio3 severely impairs skeletal muscle regeneration. This impairment is due to massive satellite cell apoptosis caused by exposure of activated satellite cells to the circulating TH. The execution of this proapoptotic program requires an intact FoxO3/MyoD axis, both genes positively regulated by intracellular TH. Thus, D3 is dynamically exploited in vivo to chronically attenuate TH signaling under basal conditions while also being available to acutely increase gene programs required for satellite cell lineage progression.
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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.