Abstract
The heart is one of the principal targets of thyroid hormones (TH) action, affecting cardiac contractility, heart rate, and diastolic function. Oxidative damage is pivotal for onset and development of cardiovascular disease (CVD) and heart failure. Specifically, free radical generation is associated to hyper-metabolic state in hyperthyroidism, whereas hypo-metabolic state induced by hypothyroidism leads to a decrease of oxidative stress. In the present review, the role of oxidative damage in CVD and failing heart-TH interplay will be considered. The main oxidative events leading to cardiac dysfunction and TH cardiac regulation at genomic and non-genomic levels will be discussed, as well as role of TH in cardioprotection and reversion of cardiac remodeling.
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