ArticleRedox biology2019
The thyroid hormone activating enzyme, type 2 deiodinase, induces myogenic differentiation by regulating mitochondrial metabolism and reducing oxidative stress.
Article in Redox biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 56 citations in OpenAlex.
- Cell-free RNA profiling uncovers non-canonical circulating D2 transcript elevation in Bladder Cancer plasma.The journal of liquid biopsy · 2026Article
- Thyroid hormones and metabolic flexibility: tissue-specific control of energy homeostasis.Frontiers in physiology · 2026Review
- The Influence of Different Light Spectra on Broiler Chicken Endocrine Systems and Productivity.Animals : an open access journal from MDPI · 2025Review
- Impact of fluoride on thyroid function and histopathology in cyprinus carpio: Implications for aquatic ecosystems.Toxicology reports · 2025Article
- Induced Types 2 and 3 Deiodinase in Non-Thyroidal Illness Syndrome and the Implications to Critical Illness-Induced Myopathy-A Prospective Cohort Study.International journal of molecular sciences · 2025Article
- Correlation between diabetic peripheral neuropathy and thyroid hormone sensitivity in elderly patients with type 2 diabetes mellitus.World journal of diabetes · 2025Article
- Genetic associations of plasma metabolites with immune cells in hyperthyroidism revealed by Mendelian randomization and GWAS-sc-eQTLs xQTLbiolinks analysis.Scientific reports · 2025Article
- Muscle PGC-1α Overexpression Drives Metabolite Secretion Boosting Subcutaneous Adipocyte Browning.Journal of cellular physiology · 2025Article
- Effect of Empagliflozin on Serum Levels of Thyroid Hormones Among Prediabetic and Diabetic Patients.International journal of endocrinology · 2025Article
- The Correlation Between Impaired Thyroid Hormone Sensitivity and Diabetic Nephropathy in Euthyroid Patients with Type 2 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Article
- Effects of thyroid hormone on monochromatic light combinations mediate skeletal muscle fiber pattern in broilers.Poultry science · 2024Article
- 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
- Metabolic differences in MSTN and FGF5 dual-gene edited sheep muscle cells during myogenesis.BMC genomics · 2024Article
- Se Alleviated Pb-Caused Neurotoxicity in Chickens:Antioxidants (Basel, Switzerland) · 2024Article
- Impaired Sensitivity to Thyroid Hormones is Associated with the Risk of Diabetic Nephropathy in Euthyroid Patients with Type 1 Diabetes Mellitus.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- Article
- Expressions of mitochondria-related genes in pregnant women with subclinical hypothyroidism, and expressions of miRNAs in maternal and cord blood.Thyroid research · 2023Article
- ApoE expression in macrophages communicates immunometabolic signaling that controls hyperlipidemia-driven hematopoiesis & inflammation via extracellular vesicles.Journal of extracellular vesicles · 2023Article
- Thyroid Hormone Regulates the Lipid Content of Muscle Fibers, Thus Affecting Physical Exercise Performance.International journal of molecular sciences · 2023Article
- Loss of p53 activates thyroid hormone via type 2 deiodinase and enhances DNA damage.Nature communications · 2023Article
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
Thyroid hormone (TH) is a key metabolic regulator that acts by coordinating short- and long-term energy needs. Accordingly, significant metabolic changes are observed depending on thyroid status. Although it is established that hyperthyroidism augments basal energy consumption, thus resulting in an enhanced metabolic state, the net effects on cellular respiration and generation of reactive oxygen species (ROS) remain unclear. To elucidate the effects of augmented TH signal in muscle cells, we generated a doxycycline-inducible cell line in which the expression of the TH-activating enzyme, type 2 deiodinase (D2), is reversibly turned on by the "Tet-ON" system. Interestingly, increased intracellular TH caused a net shift from oxidative phosphorylation to glycolysis and a consequent increase in the extracellular acidification rate. As a result, mitochondrial ROS production, and both the basal and doxorubicin-induced production of cellular ROS were reduced. Importantly, the expression of a set of antioxidant genes was up-regulated, and, among them, the mitochondrial scavenger Sod2 was specifically induced at transcriptional level by D2-mediated TH activation. Finally, we observed that attenuation of oxidative stress and increased levels of SOD2 are key elements of the differentiating cascade triggered by TH and D2, thereby establishing that D2 is essential in coordinating metabolic reprogramming of myocytes during myogenic differentiation. In conclusion, our findings indicate that TH plays a key role in oxidative stress dynamics by regulating ROS generation. Our novel finding that TH and its intracellular metabolism act as mitochondrial detoxifying agents sheds new light on metabolic processes relevant to muscle physiology.
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