ArticleProceedings of the National Academy of Sciences of the United States of America2006
Cardiac-specific elevations in thyroid hormone enhance contractility and prevent pressure overload-induced cardiac dysfunction.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.
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Who cites it
52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.
- Amiodarone and thyroid physiology, pathophysiology, diagnosis and management.Trends in cardiovascular medicine · 2019Pooled it
- American Thyroid Association Guide to investigating thyroid hormone economy and action in rodent and cell models.Thyroid : official journal of the American Thyroid Association · 2014Guideline
- Mechanical unloading is accompanied by reverse metabolic remodelling in the failing heart: Identification of a novel citraconate-mediated pathway.European journal of heart failure · 2025Article
- Metabolic Syndrome, Thyroid Dysfunction, and Cardiovascular Risk: The Triptych of Evil.International journal of molecular sciences · 2024Review
- Regression of cardiac hypertrophy in health and disease: mechanisms and therapeutic potential.Nature reviews. Cardiology · 2023Review
- Thyroid Hormone and Heart Failure: Charting Known Pathways for Cardiac Repair/Regeneration.Biomedicines · 2023Review
- Article
- Low Free Triiodothyronine as a More Sensitive Predictor of Survival Than Total Testosterone among Dialysis Men.Nutrients · 2023Article
- Short-term Changes in Thyroid-Stimulating Hormone Level after Body Fat Reduction via Partial Meal Replacement.Korean journal of family medicine · 2023Article
- Role of miR-133/Dio3 Axis in the T3-Dependent Modulation of Cardiac mitoK-ATP Expression.International journal of molecular sciences · 2022Article
- Whole-body endothermy: ancient, homologous and widespread among the ancestors of mammals, birds and crocodylians.Biological reviews of the Cambridge Philosophical Society · 2022Article
- Effect of hypothyroidism on contractile performance of isolated end-stage failing human myocardium.PloS one · 2022Article
- Selenoprotein DIO2 Is a Regulator of Mitochondrial Function, Morphology and UPRmt in Human Cardiomyocytes.International journal of molecular sciences · 2021Article
- Monoamine Oxidases Desensitize Intracellular βCirculation research · 2021Article
- The Impact of Selenium Deficiency on Cardiovascular Function.International journal of molecular sciences · 2021Review
- Deiodinases and the Three Types of Thyroid Hormone Deiodination Reactions.Endocrinology and metabolism (Seoul, Korea) · 2021Review
- Prognostic role of hypothyroidism and low free-triiodothyronine levels in patients hospitalized with acute heart failure.Internal and emergency medicine · 2021Article
- Cardiac retinoic acid levels decline in heart failure.JCI insight · 2021Article
- FoxO1-Dio2 signaling axis governs cardiomyocyte thyroid hormone metabolism and hypertrophic growth.Nature communications · 2020Article
- Maternal and fetal thyroid dysfunction following porcine reproductive and respiratory syndrome virus2 infection.Veterinary research · 2020Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
Abstract
Thyroid hormone (TH) is critical for cardiac development and heart function. In heart disease, TH metabolism is abnormal, and many biochemical and functional alterations mirror hypothyroidism. Although TH therapy has been advocated for treating heart disease, a clear benefit of TH has yet to be established, possibly because of peripheral actions of TH. To assess the potential efficacy of TH in treating heart disease, type 2 deiodinase (D2), which converts the prohormone thyroxine to active triiodothyronine (T3), was expressed transiently in mouse hearts by using the tetracycline transactivator system. Increased cardiac D2 activity led to elevated cardiac T3 levels and to enhanced myocardial contractility, accompanied by increased Ca(2+) transients and sarcoplasmic reticulum (SR) Ca(2+) uptake. These phenotypic changes were associated with up-regulation of sarco(endo)plasmic reticulum calcium ATPase (SERCA) 2a expression as well as decreased Na(+)/Ca(2+) exchanger, beta-myosin heavy chain, and sarcolipin (SLN) expression. In pressure overload, targeted increases in D2 activity could not block hypertrophy but could completely prevent impaired contractility and SR Ca(2+) cycling as well as altered expression patterns of SERCA2a, SLN, and other markers of pathological hypertrophy. Our results establish that elevated D2 activity in the heart increases T3 levels and enhances cardiac contractile function while preventing deterioration of cardiac function and altered gene expression after pressure overload.
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Registered trials
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