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Netose as a modulator of cardiac remodeling after myocardial infarction

Grant number: 14/26564-0
Support type:Scholarships in Brazil - Post-Doctorate
Effective date (Start): April 01, 2015
Effective date (End): March 31, 2018
Field of knowledge:Health Sciences - Medicine
Cooperation agreement: Coordination of Improvement of Higher Education Personnel (CAPES)
Principal Investigator:Leonardo Antonio Mamede Zornoff
Grantee:Tatiana Fernanda Bachiega Pinelli
Home Institution: Faculdade de Medicina (FMB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil

Abstract

Cardiac remodeling after acute myocardial infarction is related to progression of ventricular dysfunction and represents an important therapeutic target in heart failure due different etiologies. Among the complex mechanisms activated postinfarction that modulate the remodeling process, the inflammatory response appears as an important predictor of left ventricular remodeling. In this context, the role of neutrophils deserves further investigation as the increased in the count of these cells itself is a prognostic biomarker of left ventricular cardiac remodeling. In addition, neutrophils are associated with larger infarct size and significant worsening of cardiac function. Therefore, the involvement of neutrophils in myocardial injury induced by myocardial infarction and cardiac remodeling is consistent, but the exact mechanisms by which these interactions occurs remains understudied. In this sense, the NETs (neutrophil extracellular traps) recently described structures, first related to microbicidal activity against various pathogens classes has gained ground on the cardiovascular research, and has been demonstrated the relationship between NETs and the beginning of atherosclerosis in the carotid arteries, and promote the growth and stabilization of thrombi in infarction patients. The NETs comprising extruding cytoplasmic and nuclear materials of neutrophils to the extracellular medium, network format, and these structures enable the extracelular action of various factors such as DNA, histone, elastase among others. Understanding the role of neutrophils and consequently of NETs in remodeling may set precedents for future interventions to improve the prognosis of patients. However, relevant aspect to be considered is that there are no data in the literature regarding the influence of NETs in cardiac remodeling secondary to myocardial infarction. Therefore, our objective is to study the role of NETs on cardiac remodeling after myocardial infarction. (AU)