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The crosstalk between thyroid hormones and inflammatory processes might be relevant in the context of cardioprotection. Continuous activation of the inflammatory system in myocytes has dangerous effects and,importantly, thyroid hormones can modulate the inflammatory and immune response through genomic and nongenomic mechanisms. The nongenomic action of thyroid hormones depends, at least in part, on the interaction with the plasma membrane receptor integrin αvβ3 (to which T4 has a higher affinity than T3 )and the relationship between inflammatory markers and thyroid hormones seems to be mediated through this receptor. In vitro studies have shown that T3 induces an increase in interleukin (IL)-6 and IL‑8 in human osteoblastic-like cells and human bone marrow stromal cells238, whereas in murine dendritic cells, T3 increased IL‑12 but not IL‑10 . Notably, in the study in human cells, a supraphysiological dose of T3 (10 nmol/l) was required to obtain the effect, while physiological doses did not induce a response.

In the HF setting, the continuous activation of the inflammatory system changes the protective adaptive role of immune responses. Instead of immune responses that promote resistance to myocardial hypoxic injury and induce extracellular matrix remodelling and cell proliferation240,241, chronic inflammation leads to dangerous effects for the heart with the induction of apoptosis in myocytes and endothelial cells and, therefore, favouring HF progression242. In patients with HF, levels of IL‑6 and TNF correlated inversely with those of free T3, but not with levels of free T4 and TSH243. Low T3 circulating levels might depend on inhibition of the peripheral conversion of T4 into T3 following the inhibition of the type 5ʹ deiodinase activity244. Although we cannot exclude the possibility that thyroid hormones might be a permissive factor in inflammatory conditions of the heart (pericarditis and myocarditis), additional and more substantial data are necessary.