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Updated: Mar 22, 2026
Author Spotlight: In Vivo Assessment of Thyroid Hormone Disruption Using the THAI Mouse Model
Published on: October 6, 2023
Tissue thyroid hormones and thyronamines
Alice Accorroni1, Federica Saponaro1, Riccardo Zucchi2
1Scuola Superiore Sant'Anna, Pisa, Italy.
Insights
Thyroid hormones significantly impact heart function. This review details how thyroxine (T4) and triiodothyronine (T3), along with metabolites like T2 and T1AM, influence cardiac physiology and pathophysiology.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Thyroid disease profoundly affects cardiac function, with hyperthyroidism causing increased heart rate and hypothyroidism leading to decreased contractility.
- Recent research offers new insights into thyroid hormone regulation of the heart.
Purpose of the Study:
- To review current knowledge on thyroid hormone (T4, T3) transport, metabolism, and their genomic/non-genomic effects on the heart.
- To discuss specific cardiac implications, including calcium homeostasis, pacemaker activity, and metabolic effects of thyroid hormone metabolites.
Main Methods:
- Literature review focusing on thyroid hormone physiology, pathophysiology, and cardiac regulation.
- Analysis of genomic and non-genomic signaling pathways influenced by T3, T2, and T1AM.
Main Results:
- Thyroid hormones regulate cardiac proteins involved in calcium homeostasis and pacemaker cell activity via genomic and non-genomic pathways.
- Metabolites T2 and T1AM stimulate fatty acid oxidation; T1AM exhibits negative inotropic/chronotropic effects at high concentrations and potential cardioprotection at physiological levels.
- D3 deiodinase induction in heart failure may cause cardiac hypothyroidism, with controversial clinical implications.
- T3 and thyroid hormone receptor α1 play roles in post-infarction repair.
Conclusions:
- Thyroid hormones and their metabolites have complex, multifaceted effects on cardiac function, ranging from metabolic regulation to cardioprotection.
- Understanding these mechanisms is crucial for managing thyroid disease-related cardiac conditions and exploring therapeutic strategies.
Abstract:
It has been known for a long time that changes in cardiac function are a major component of the clinical presentation of thyroid disease. Increased heart rate and hyperdynamic circulation are hallmarks of hyperthyroidism, while bradycardia and decreased contractility characterize hypothyroidism. Recent findings have provided novel insights in the physiology and pathophysiology of heart regulation by thyroid hormones. In this review, we summarize the present knowledge on thyroxine (T4) transport and metabolism and on the biochemical pathways leading to genomic and non-genomic effects produced by 3,5,3'-triiodothyronine (T3) and by its active metabolites, particularly 3,5-diiodothyronine (T2) and 3-iodothyronamine (T1AM). On this basis, specific issues of special interest for cardiology are discussed, namely (1) relevance of the regulation of proteins involved in the control of calcium homeostasis and in pacemaker cell activity, due to non-genomic as well as to classical genomic effects; (2) stimulation of fatty acid oxidation by T2 and T1AM, the latter also causing a negative inotropic and chronotropic action at micromolar concentrations; (3) induction of D3 deiodinase in heart failure, potentially causing selective cardiac hypothyroidism, whose clinical implications are still controversial; and (4) cardioprotective effect of T1AM, possibly occurring at physiological concentrations, and relevance of T3 and of thyroid hormone receptor α1 in post-infarction repair.
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