Cardiac remodeling (CR) is a time dependent process that promotes cellular and molecular changes that are clinically manifested by changes in size, shape and function of the myocardium after injure, and heart failure (HF) is the final stage of this process. Heart failure is characterized by impaired perfusion of blood from the heart to other body tissues. This is due, in part, by the presence of hypertrophy and fibrosis that occurs in cardiomyocytes, which decrease their driving activity of the heart. MicroRNAs, molecules involved in the regulation of pro and anti-inflammatory responses in hypertrophic growth and extracellular matrix deposition are also involved in the HF. However, little is known about the role of these small molecules in cardiac muscle from dysfunction to HF. The aim of this study is to evaluate structural and molecular aspects of the heart muscle from dysfunction to HF, in an induced aortic stenosis (AS) model. 32 male Wistar rats (90 to 100g) will be used. After 18 and 28 weeks of surgery induction of AS, control animals (Sham) and AS will be submitted to echocardiography to assess ventricular function and sacrificed to collect samples of the left ventricle, most affected by the HF, for histochemical and molecular analysis. Picrosirius for morphology analysis and quantification of collagen in the extracellular matrix will be performe. The analysis of gene expression of collagen types 1A1, 1A2 and Col. 3 and miRNA 29b will be achieved by RT- qPCR. The results may help in the characterization of genes and miRNAs expressed from dysfunction to HF in the cardiac muscle and point out important miRNAs in the regulation of genes involved in the progression of HF.
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