Impact of hyperthyroidism on cardiac hypertrophy

The cardiac growth process (hypertrophy) is a crucial phenomenon conserved across a wide array of species and is critically involved in the maintenance of cardiac homeostasis. This process enables an organism to adapt to changes in systemic demand and occurs due to a plethora of responses, depending...

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Bibliographic Details
Published in:	Endocrine Connections Vol. 9; no. 3; pp. R59 - R69
Main Authors:	Barreto-Chaves, M L M, Senger, N, Fevereiro, M R, Parletta, A C, Takano, A P C
Format:	Journal Article
Language:	English
Published:	England Bioscientifica Ltd 01-03-2020 Bioscientifica
Subjects:	cardiac myocyte cardiac remodeling molecular mechanisms renin-angiotensin system Review thyroid hormones molecular mechanisms cardiac myocyte renin-angiotensin system thyroid hormones cardiac remodeling
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Summary:	The cardiac growth process (hypertrophy) is a crucial phenomenon conserved across a wide array of species and is critically involved in the maintenance of cardiac homeostasis. This process enables an organism to adapt to changes in systemic demand and occurs due to a plethora of responses, depending on the type of signal or stimuli received. The growth of cardiac muscle cells in response to environmental conditions depends on the type, strength and duration of stimuli, and results in adaptive physiological responses or non-adaptive pathological responses. Thyroid hormones (TH) have a direct effect on the heart and induce a cardiac hypertrophy phenotype, which may evolve to heart failure. In this review, we summarize the literature on TH function in the heart by presenting results from experimental studies. We discuss the mechanistic aspects of TH associated with cardiac myocyte hypertrophy, increased cardiac myocyte contractility and electrical remodeling, as well as the associated signaling pathways. In addition to classical crosstalk with the sympathetic nervous system (SNS), emerging work pointing to the new endocrine interaction between TH and the renin-angiotensin system (RAS) is also explored. Given the inflammatory potential of the angiotensin II peptide, this new interaction may open the door for new therapeutic approaches which target the key mechanisms responsible for TH-induced cardiac hypertrophy.
Bibliography:	ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1
ISSN:	2049-3614 2049-3614
DOI:	10.1530/EC-19-0543