he heart is a muscular organ with capacity for remodeling. The increased plasma levels of thyroid hormones (TH) trigger myocardial hypertrophy response and lead to impaired contractile function and heart failure. The development of cardiac hypertrophy is a major risk factor for cardiovascular morbidity and mortality in hyperthyroidism and occurs initially as adaptive response to the workload generated by hemodynamic changes, as well as by direct action of thyroid hormones on protein synthesis myocardium. Although in vivo and in vitro studies have demonstrated the involvement of the enzyme PI3K/Akt/mTOR in thyroid hormone induced cardiac hypertrophy, little is known about CaN/NFAT and MEF2/HDACs. The alteration in the function and expression of regulatory proteins of intracellular Ca2+ is a frequent feature in different models of cardiac hypertrophy, however, the participation of Ca2+ as critical mediator of cardiomyocyte growth observed in hyperthyroidism remains unknown. Since cardiac hypertrophy and heart failure have been considered a major problem in cardiovascular pathophysiology nowadays, the identification of the molecular basis related to these processes may result in new therapeutic strategy to help improve cardiomyopathy. In this context, our aim is to evaluate the contribution of Ca2+ dependent signaling pathways, CaN/NFAT and MEF2/HDACs, in thyroid hormone-induced cardiac hypertrophy in vitro and the possible renin-angiotensin system involvement, which is activated in hyperthyroidism.
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