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First published online on January 4, 2005
This version published online on July 7, 2005
Endocrine Reviews, doi:10.1210/er.2003-0033
Endocrine Reviews, doi:10.1210/er.2003-0033
Endocrine Reviews 0 (2005): 200300332-
Copyright © 2005 by The Endocrine Society
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Thyroid Hormone Action in the Heart

George J. Kahaly and Wolfgang H. Dillmann*

Department of Medicine I (G.J.K.), Endocrine Unit, Gutenberg-University Hospital, Mainz, D-55101 Germany; and Department of Medicine (W.H.D.), Division of Endocrinology & Metabolism, University of California, San Diego, La Jolla, California 92093-0618

* To whom correspondence should be addressed. E-mail: wdillmann{at}ucsd.edu.

The heart is a major target organ for thyroid hormone action, and marked changes occur in cardiac function in patients with hypo- or hyperthyroidism. T3-induced changes in cardiac function can result from direct or indirect T3 effects. Direct 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. T3 also leads to an increase in the speed of diastolic relaxation, which is caused by the more efficient pumping of the calcium ATPase of the sarcoplasmic reticulum. This T3 effect results from T3-induced increases in the level of the mRNA coding for the sarcoplasmic reticulum calcium ATPase protein, leading to an increased number of calcium ATPase pump units in the sarcoplasmic reticulum.




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