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Impact of NLRP3 inflammasome in the morphological and functional cardiac alterations induced by hyperthyroidism and sympathetic activation

Grant number: 21/06556-7
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): August 01, 2021
Effective date (End): July 31, 2022
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal researcher:Maria Luiza de Morais Barreto de Chaves
Grantee:Felipe Silva Saltão
Home Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Associated research grant:19/17031-2 - Inflammasome in the cardiac physiopathology, AP.TEM


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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