Impact of NLRP3 inflammasome in the cardiac hypertrophy models induced by T3 and by isoproterenol

Abstract

We have previously demonstrated that T3 induces to increased S100A8 levels, a DAMP involved with TLR4/MyD88/NF-kB signaling and important to cardiac hypertrophy observed in hyperthyroidism. This signaling pathway is critical to activation of intracellular sensors as NLRP3, AIM2, NLRC4 and inlammasome activation. On the other hand, beta-adrenergic stimulation also acts in the NF-kB signaling, but the role of inlammasome in this condition remains to be clarified. In addition, beta-adrenergic stimulation leads to increased myocardial contractility by mechansims related to calcium, which can represent a DAMP and then activating inflammasome. The objective of this study is to evaluate in murine model the role of NLRP3, ASC and Caspase-1 in both cardiac hypertrophy models. (AU)