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M L M Barreto-Chaves, N Senger, M R Fevereiro, A C Parletta and A P C Takano

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.

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Tsuneo Ogawa and Adolfo J de Bold

natriuretic peptide coexist in the secretory granules of human cardiac myocytes . American Journal of Hypertension 1991 4 909 – 912 . ( doi:10.1093/ajh/4.2.113 ). 20 Kojima M Minamino N Kangawa K Matsuo H

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Madalena von Hafe, João Sergio Neves, Catarina Vale, Marta Borges-Canha and Adelino Leite-Moreira

contractile apparatus of the cardiac myocyte has two subtypes of myosin heavy chains (MHCs): α-MHC and β-MHC – fast and slow myosin, respectively. T3 can upregulate α-MHC and downregulate β-MHC ( 10 ). Therefore, the myocardial hypothyroid state induces a so

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Frans H H Leenen, Mordecai P Blaustein and John M Hamlyn

+ concentrations . Journal of Biological Chemistry 2000 275 27838 – 27844.  99 Liu L Zhao X Pierre SV Askari A. Association of P13K-Akt signaling apthway with digitalis-induced hypertrophy of cardiac myocytes . American Journal of

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Adriana J van Ballegooijen, Marjolein Visser, Marieke B Snijder, Jacqueline M Dekker, Giel Nijpels, Coen D A Stehouwer, Michaela Diamant and Ingeborg A Brouwer

:10.1111/j.1753-4887.2008.00100.x ). 2 Nibbelink KA Tishkoff DX Hershey SD Rahman A Simpson RU . 1,25(OH)2-vitamin D3 actions on cell proliferation, size, gene expression, and receptor localization, in the HL-1 cardiac myocyte . Journal of

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Flavia Letícia Martins Peçanha, Reinaldo Sousa dos Santos and Wagner Seixas da-Silva

2008 149 6462 – 6470 . ( doi:10.1210/en.2008-0202 ) 41 Iordanidou A Hadzopoulou-Cladaras M Lazou A . Non-genomic effects of thyroid hormone in adult cardiac myocytes: relevance to gene expression and cell growth . Molecular and

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Vito Francic, Martin Keppel, Verena Schwetz, Christian Trummer, Marlene Pandis, Valentin Borzan, Martin R Grübler, Nicolas D Verheyen, Marcus E Kleber, Graciela Delgado, Angela P Moissl, Benjamin Dieplinger, Winfried März, Andreas Tomaschitz, Stefan Pilz and Barbara Obermayer-Pietsch

analysis ( 16 ). Moreover, studies on primary human cells have shown that sST2 is predominantly secreted by lung epithelial cells and cardiac myocytes ( 17 ), while several other cell types, such as venous and arterial endothelial cells ( 18 ), as well as

Open access

K Amrein, A Papinutti, E Mathew, G Vila and D Parekh

, binding to vitamin D receptors (VDR) on cardiac myocytes and furthermore by having antioxidant properties that may reduce levels of reactive oxygen species (ROS) in the atria, which contribute to inflammation and proarrhythmic substrate formation ( 79