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

Grant number: 21/04817-8
Support type:Scholarships in Brazil - Post-Doctorate
Effective date (Start): June 01, 2021
Effective date (End): May 31, 2023
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal researcher:Maria Luiza de Morais Barreto de Chaves
Grantee:Karine Panico
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 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)

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