Tissue thyroid hormones and thyronamines
Open accessAbstract
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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3,5-T2 concentrations in cardiac rodent tissue were found to be below detection limits in a study aiming to determine THM concentrations in rat heart.
“3,5-T2 concentrations in cardiac rodent tissue were found to be below detection limits (100) in a study aiming to determine THM concentrations in rat heart.”
From 3,5-T2—A Janus-Faced Thyroid Hormone Metabolite Exerts Both Canonical T3-Mimetic Endocrine and Intracrine Hepatic Action (2020) · cites this paper as [100]
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Saponaro, F., Sestito, S., Runfola, M., Rapposelli, S., & Chiellini, G. (2020) · Frontiers in Medicine · doi:10.3389/fmed.2020.00331 · Cited by 124 · see citing works
Self-citationThyroid hormone resistance: mechanisms and therapeutic development
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- Authors
- Accorroni, A., Saponaro, F., & Zucchi, R.
- Affiliations
- Scuola Superiore Sant'Anna (IT)
- University of Pisa (IT)
- Corresponding author
- Zucchi, Riccardo
- Venue
- Heart Failure Reviews
- Published
- 2016-04-26
- Volume
- 21
- Issue
- 4
- Pages
- 373-390
- ISSN
- 1382-4147 (ISSN-L)
- 1573-7322
- OpenAlex
- W2343803740
- Cited by
- 29
- References
- 13
- Citations by year
- 2024: 2 · 2023: 1 · 2022: 3 · 2021: 4 · 2020: 7 · 2019: 4 · 2018: 3 · 2017: 5
- FWCI
- 0.56
- Type
- journal article
- Language
- en
- Open access
- green
- link.springer.com
- Licence
- other-oa
- www.springer.com/tdm (tdm)
- Locations
- Heart Failure Reviews (publishedVersion)
- PubMed (publishedVersion)
- CINECA IRIS Institutial research information system (University of Pisa) (submittedVersion, other-oa)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Cancer Diagnosis and Treatment
- Keywords
- thyroid hormones, thyronamines, 3,5-diiodothyronine, 3-iodothyronamine, triiodothyronine, thyroxine transport, cardiac function, hyperthyroidism, hypothyroidism, calcium homeostasis, pacemaker cells, fatty acid oxidation, inotropic and chronotropic effects, type 3 deiodinase, heart failure, cardioprotection, thyroid hormone receptor alpha 1
- MeSH terms
- Animals, Disease Models, Animal, Heart, Heart Failure, Humans, Hyperthyroidism, Hypothyroidism, Thyroid Hormones, Lipid Metabolism, Mice, Rats
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