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Inflammasome in the cardiac physiopathology

Grant number: 19/17031-2
Support Opportunities:Research Projects - Thematic Grants
Duration: October 01, 2020 - September 30, 2025
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Maria Luiza de Morais Barreto de Chaves
Grantee:Maria Luiza de Morais Barreto de Chaves
Host Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Associated researchers:Ana Paula Cremasco Takano ; Carolina Demarchi Munhoz ; Cláudio Romero Farias Marinho ; Sudhiranjan Gupta ; Vagner Roberto Antunes
Associated scholarship(s):23/02235-7 - Impact of NLRP3 inflammasome in the cardiac hypertrophy models induced by T3 and by isoproterenol, BP.PD
22/00057-1 - Potential cardioprotective role of angiotensin II receptor type 2 (AT2) in aging-associated cardiac senescence: possible involvement of inflammasomes, BP.MS
22/05156-8 - Technical support in the maintenance of transgenic animal lines related to the investigation of inflammasomes in the animal facility of the Department of Anatomy., BP.TT
+ associated scholarships 22/00840-8 - Role of the caspase-1 in age-associated cardiac changes (structural and functional). Possible involvement of the AIM2 inflammasome, BP.PD
21/06151-7 - Role of NLRP3 inflammasome on the cardiac function in Hypothyroid animals, BP.DD
21/06556-7 - Impact of NLRP3 inflammasome in the morphological and functional cardiac alterations induced by hyperthyroidism and sympathetic activation, BP.IC
21/04817-8 - Impact of NLRP3 inflammasome in the cardiac hypertrophy models induced by T3 and by isoproterenol, BP.PD - associated scholarships


Cardiovascular diseases remain the leading cause of global morbidity and mortality today. Even considering the scientific and technological advances of the last two decades, it is estimated that in 2030 more than 23 million people will die due to cardiovascular diseases. Although different stimuli may induce heart failure (HF), it is preceded by cardiac hypertrophy, characterized by increased cardiomyocyte volume and consequently increased left ventricle thickness. Several groups, including ours, have been demonstrating that, like other chronic diseases, the cardiomyocyte hypertrophic phenotype is associated to mechanisms related to inflammation. Thus, there is a growing interest today in investigating which contribution and what specific local stimuli in the "cardiomyocyte environment" are responsible for the activation of specific signaling pathways selectively implicated in the transition from adaptive/compensated cardiac hypertrophy to a decompensated/pathologic phenotype, leading to HF. Then, the identification of new signaling pathways and mechanisms responsible for the activation of inflammatory factors associated to HF, such as IL-1² and IL-18, may contribute to new therapeutic targets resulting in slower progression of disease. After synthesized in cardiac cells, these inflammatory factors are activated via inflammassome, a multi-protein complex formed by different elements (NLRs, ASC and Caspase-1) and then they are released to extracelular space. The hypothesis of this study is that the inflammassome may function as an important mediator in the pathogenesis of cardiac hypertrophy that precedes HF. Thus, this project aims to study the participation of NLRs, ASC adapter molecule and Caspase-1 in the pathogenesis of compensated/physiological and decompensated/pathological cardiac hypertrophy using transgenic murine models and/or human cardiomyocyte cell cultures. The knowledge acquired about aspects involving the innate immune responses will contribute for our understanding concerning mechanisms related to the progression of cardiac hypertrophy, besides enabling studies directed to the development of new methodologies and therapeutic strategies that attenuate progression to HF. (AU)

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