ArticleMolecular endocrinology (Baltimore, Md.)2005
Thyroid hormone induces cardiac myocyte hypertrophy in a thyroid hormone receptor alpha1-specific manner that requires TAK1 and p38 mitogen-activated protein kinase.
Article in Molecular endocrinology (Baltimore, Md.), 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 80 citations in OpenAlex.
- Predicting major cardiac and cerebrovascular events in acute coronary syndrome patients using the thyroid hormone sensitivity index.Frontiers in endocrinology · 2025Article
- Cardiac recovery from pressure overload is not altered by thyroid hormone status in old mice.Frontiers in endocrinology · 2024Article
- Circulating thyroid hormones and clinical parameters of heart failure in men.Scientific reports · 2023Article
- TRα2-An Untuned Second Fiddle or Fine-Tuning Thyroid Hormone Action?International journal of molecular sciences · 2022Review
- Thyroid hormone-dependent regulation of metabolism and heart regeneration.The Journal of endocrinology · 2022Review
- Endocrine Influence on Cardiac Metabolism in Development and Regeneration.Endocrinology · 2021Review
- Thyroid hormone signaling and consequences for cardiac development.The Journal of endocrinology · 2019Review
- The impact of thyroid hormone dysfunction on ischemic heart disease.Endocrine connections · 2019Review
- Thyroid hormone receptor function in maturing ovine cardiomyocytes.The Journal of physiology · 2019Article
- Maternal chromium restriction modulates miRNA profiles related to lipid metabolism disorder in mice offspring.Experimental biology and medicine (Maywood, N.J.) · 2017Article
- Role of the Thyroid System in the Dynamic Complex Network of Cardioprotection.European cardiology · 2016Review
- Cardioprotection and thyroid hormones.Heart failure reviews · 2016Review
- Role of thyroid hormones in ventricular remodeling.Current heart failure reports · 2015Review
- Thyroid hormone does not induce maturation of embryonic chicken cardiomyocytes in vitro.Physiological reports · 2014Article
- Unexpected maturation of PI3K and MAPK-ERK signaling in fetal ovine cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2014Article
- Thyroid hormone regulation of metabolism.Physiological reviews · 2014Review
- The emerging role of TRα1 in cardiac repair: potential therapeutic implications.Oxidative medicine and cellular longevity · 2014Review
- Inhibition of thyroid hormone receptor α1 impairs post-ischemic cardiac performance after myocardial infarction in mice.Molecular and cellular biochemistry · 2013Article
- Genetic evidence that thyroid hormone is indispensable for prepubertal insulin-like growth factor-I expression and bone acquisition in mice.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2012Article
- Dose-dependent effects of thyroid hormone on post-ischemic cardiac performance: potential involvement of Akt and ERK signalings.Molecular and cellular biochemistry · 2012Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alterations in TR [thyroid hormone (TH) receptor]1 isoform expression have been reported in models of both physiologic and pathologic cardiac hypertrophy as well as in patients with heart failure. In this report, we demonstrate that TH induces hypertrophy as a direct result of binding to the TRalpha1 isoform and, moreover, that overexpression of TRalpha1 alone is also associated with a hypertrophic phenotype, even in the absence of ligand. The mechanism of TH and TRalpha1-specific hypertrophy is novel for a nuclear hormone receptor and involves the transforming growth factor beta-activated kinase (TAK1) and p38. Mitigating TRalpha1 effects, both TRalpha2 and TRbeta1 attenuate TRalpha1-induced myocardial growth and gene expression by diminishing TAK1 and p38 activities, respectively. These findings refine our previous observations on TR expression in the hypertrophied and failing heart and suggest that manipulation of thyroid hormone signaling in an isoform-specific manner may be a relevant therapeutic target for altering the pathologic myocardial program.
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