We have demonstrated that T3 induces to increased S100A8, a DAMP which activates TLR4/MyD88/NF-kB signaling pathway and essential to cardiac hypertrophy observed in the hyperthyroidism. This signaling pathway is critical to activate different intracellular sensors such as NLRP3, AIM2, NLRC4 and other inflammasomes. Beta-adrenergic stimulation also activates NF-kB, although there are no reports on the role of the inflammasome in the myocardium under these conditions. It is noteworthy that, beta-adrenergic stimulation in the cardiomyocyte, through beta-2 type receptors, increases its contractility by mechanisms involving intracellular calcium elevation, which can act as DAMP activating the inflammasome, allowing us to hypothesize that in this model there may be participation of this protein complex. The main objective of this study is to evaluate, in a murine model, the role of innate receptors NLRP3, of the adapter molecule ASC and of Caspase-1, in two distinct models of cardiac hypertrophy (by T3 and by isoproterenol), evaluating morphological aspects (through histological analysis) and hemodynamic parameters (heart rate and tail pressure).
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