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Updated: Aug 15, 2026

In vivo Characterization of Endocrine Disrupting Chemical Effects via Thyroid Hormone Action Indicator Mouse
Published on: October 6, 2023
[Cellular mechanisms of thyroid hormone action]
S Vinzio1, O Morel, J-L Schlienger
1Service de médecine interne et nutrition, Hôpital Hautepierre, av. Molière, 67098 Strasbourg cedex 67, France. stephane.vinzio@chru-strasbourg.fr
Key Points:
Thyroid hormones affect cardiac myocytes as well as the smooth muscle and endothelial cells of the vascular wall. Free 3,53'-L-triiodothyronine (FT3) and its specific nuclear receptor modulate the transcription of various proteins, principally those involved in the myocyte contractile apparatus (myosin heavy chains), and the regulation of intracellular calcium flux (sarcoplasmic reticulum Ca2+ATPase). Thyroid hormones also have non-genomic effects that work rapidly, complement the effects described above, and are related to alterations in the properties of many channels and membrane receptors, especially in the sinoatrial mode. Thyroid hormones also affect the smooth muscle and endothelial cells of the vascular walls and reduce systemic vascular resistance. These effects on cardiac and vascular cells globally explain the cardiac manifestations (especially the inotropic and chronotropic effects) observed during dysthyroidism, particularly in hyperthyroidism where they are often in the forefront (positive inotropic and chronotropic effects).
Insights
Thyroid hormones, including free 3,53'-L-triiodothyronine (FT3), impact heart and blood vessel cells. These hormones influence cardiac contractility and vascular resistance, explaining symptoms seen in thyroid dysfunction like hyperthyroidism.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Molecular Biology
Background:
- Thyroid hormones are crucial regulators of cellular function.
- Cardiac myocytes and vascular cells are key targets of thyroid hormone action.
- Dysregulation of thyroid hormones leads to significant cardiovascular manifestations.
Purpose of the Study:
- To elucidate the molecular mechanisms by which thyroid hormones affect cardiac and vascular cells.
- To explain the cardiac manifestations associated with thyroid dysfunction, particularly hyperthyroidism.
Main Methods:
- Analysis of genomic and non-genomic effects of thyroid hormones.
- Investigation of protein modulation, including myosin heavy chains and Ca2+ATPase.
- Examination of effects on ion channels and membrane receptors in cardiac and vascular cells.
Main Results:
- Free 3,53 -L-triiodothyronine (FT3) and its receptor modulate key contractile proteins (myosin heavy chains) and calcium handling (sarcoplasmic reticulum Ca2+ATPase).
- Thyroid hormones exert rapid, non-genomic effects on sinoatrial node channels and receptors.
- Thyroid hormones reduce systemic vascular resistance by affecting vascular smooth muscle and endothelial cells.
Conclusions:
- Thyroid hormones significantly impact cardiac myocyte contractility and vascular tone.
- Genomic and non-genomic actions of thyroid hormones contribute to cardiovascular regulation.
- The cardiac and vascular effects of thyroid hormones provide a comprehensive explanation for clinical findings in dysthyroidism, especially hyperthyroidism.
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