New insights into mechanisms of cardioprotection mediated by thyroid hormones

Heart failure represents the final common outcome in cardiovascular diseases. Despite significant therapeutic advances, morbidityand mortality of heart failure remain unacceptably high. Heart failure is preceded and sustained by a process of structuralremodeling of the entire cardiac tissue architecture. Prevention or limitation of cardiac remodeling in the early stages of theprocess is a crucial step in order to ameliorate patient prognosis. Acquisition of novel pathophysiological mechanisms of cardiacremodeling is therefore required to develop more efficacious therapeutic strategies. Among all neuroendocrine systems, thyroidhormone seems to play a major homeostatic role in cardiovascular system. In these years, accumulating evidence shows that the"low triiodothyronine" syndrome is a strong prognostic, independent predictor of death in patients affected by both acute andchronic heart disease. In experimental models of cardiac hypertrophy or myocardial infarction, alterations in the thyroid hormonesignaling, concerning cardiac mitochondrion, cardiac interstitium, and vasculature, have been suggested to be related to heartdysfunction. The aim of this brief paper is to highlight new developments in understanding the cardioprotective role of thyroidhormone in reverting regulatory networks involved in adverse cardiac remodeling. Furthermore, new recent advances on the roleof specific miRNAs in thyroid hormone regulation at mitochondrion and interstitial level are also discussed.