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Low blood levels of the thyroid hormones — triiodothyronine (T3) and thyroxine (T4) — signal the hypothalamus to release the thyrotropin-releasing hormone (TRH). TRH then reaches the pituitary gland and stimulates the release of thyroid-stimulating hormone(TSH) into the bloodstream.
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The thyroid hormone (TH) plays a pivotal role in the intricate orchestration of physiological processes, exerting profound effects on development, metabolism, and homeostasis throughout different life stages.
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Hormones, the biochemical messengers produced by endocrine glands, are pivotal in regulating bodily functions and maintaining homeostasis. Each hormone's balance is crucial; imbalances can lead to significant physiological disruptions. Major hormones include oxytocin, cortisol, epinephrine, estrogen, testosterone, thyroxine, growth hormone, insulin, and glucagon.
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Adrenergic agonists have diverse therapeutic uses across various medical conditions and emergencies.
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Updated: Mar 22, 2026

Author Spotlight: In Vivo Assessment of Thyroid Hormone Disruption Using the THAI Mouse Model
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Author Spotlight: In Vivo Assessment of Thyroid Hormone Disruption Using the THAI Mouse Model

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Tissue thyroid hormones and thyronamines.

Alice Accorroni1, Federica Saponaro1, Riccardo Zucchi2

  • 1Scuola Superiore Sant'Anna, Pisa, Italy.

Heart Failure Reviews
|April 27, 2016
PubMed
Summary
This summary is machine-generated.

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.

Keywords:
3,5-Diiodothyronine3-IodothyronamineHeart failureIschemiaThyroid hormone

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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.