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Cited by 338Thyroid Disorders and TreatmentsCardiac electrophysiology and arrhythmiasEstrogen and related hormone effects

Biochemical basis of thyroid hormone action in the heart.

Dillmann, Wolfgang H.·1990·The American Journal of Medicine
DOI 10.1016/0002-9343(90)90530-q
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Abstract

Thyroid hormone-induced changes in cardiac function have been recognized for over 150 years; however, the biochemical basis of triiodothyronine (T3) action in the heart has been intensely investigated only during the last two decades. T3-induced changes in cardiac function can result from direct or indirect T3 effects. Direct T3 effects result from T3 action in the heart itself and are mediated by nuclear or extranuclear mechanisms. Extranuclear T3 effects, which occur independent of nuclear T3 receptor binding and increases in protein synthesis, influence primarily the transport of amino acids, sugars, and calcium across the cell membrane. Nuclear T3 effects are mediated by the binding of T3 to specific nuclear receptor proteins, which results in increased transcription of T3-responsive cardiac genes. The T3 receptor is a member of the ligand-activated transcription factor family and is encoded by cellular erythroblastosis A (c-erb A) genes. The c-erb A protein is the cellular homologue of the viral erythroblastosis A (v-erb A) protein, which causes red cell leukemia in chickens. Currently, three T3-binding isoforms of the c-erb protein and two non-T3-binding nuclear proteins that exert positive and negative effects on T3-responsive cardiac genes have been identified. T3 increases the heart transcription of the myosin heavy chain (MHC) alpha gene and decreases the transcription of the MHC beta gene, leading to an increase of myosin V1 and a decrease in myosin V3 isoenzymes.…

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  • In animal models, T3 has a positive direct inotropic effect.

    “In animal models T 3 has a positive direct inotropic effect by inducing a predominant synthesis of fast ␣-isoforms of heavy myosin chains and by increasing calcium-adenosine triphosphatase and cAMP levels, together with the number and sensitivity of ␤-adrenergic receptors (6 -10).”

    From The Role of Thyroid Hormone in Blood Pressure Homeostasis: Evidence from Short-Term Hypothyroidism in Humans (2002) · cites this paper as [6]

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Authors
Dillmann, W. H.
Affiliations
University of California San Diego (US)
Corresponding author
Dillmann, Wolfgang H.
ORCID
Dillmann, Wolfgang H.
Venue
The American Journal of Medicine
Publisher
Elsevier BV
Published
1990-06
Volume
88
Issue
6
Pages
626-630
ISSN
0002-9343 (ISSN-L)
DOI
10.1016/0002-9343(90)90530-q
OpenAlex
W2042315468
Cited by
338
References
0
Citations by year
2026: 1 · 2025: 1 · 2024: 5 · 2023: 2 · 2022: 6 · 2021: 6 · 2020: 3 · 2019: 6 · 2018: 7 · 2017: 5 · 2016: 7 · 2015: 5 · 2014: 6 · 2013: 17 · 2012: 14
FWCI
1.52
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • The American Journal of Medicine (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5r01hl025022-25)
  • National Heart, Lung, and Blood Institute (HL-25022)
Topics
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Thyroid Disorders and Treatments
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
Keywords
thyroid hormones, triiodothyronine, cardiac function, T3 receptor, c-erbA, nuclear receptors, myosin heavy chain isoforms, myosin ATPase activity, sarcoplasmic reticulum calcium ATPase, diastolic relaxation, myocardial energy metabolism, cardiac contractility
MeSH terms
Heart, Humans, Myocardium, RNA, Messenger, Transcription, Genetic, Triiodothyronine

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