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Characterization of mitochondrial metabolism and dynamics in cardiac dysfunction-induced myocardial infarction in rats: effects of exercise training

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Author(s):
Juliane Cruz Campos
Total Authors: 1
Document type: Master's Dissertation
Press: São Paulo.
Institution: Universidade de São Paulo (USP). Escola de Educação Física e Esportes (EEFE/BT)
Defense date:
Examining board members:
Julio Cesar Batista Ferreira; Patricia Chakur Brum; Francisco Rafael Martins Laurindo
Advisor: Julio Cesar Batista Ferreira
Abstract

Myocardial infarction is considered the etiology that most contributes to the onset of heart failure in humans. Among the ventricular dysfunction-associated cellular abnormalities, changes in mitochondrial function and dynamics are critical, since the organelle homeostasis is crucial in maintaining the metabolic, electrical and mechanical properties of the heart. In the present study, we characterized in cardiac dysfunction- induced myocardial infarction in rats: a) cardiac phenotype; b) mitochondrial metabolism; c) redox balance, and d) mitochondrial dynamics. Our results show that twelve weeks after myocardial surgery, the animals developed pathological cardiac remodeling-associated ventricular dysfunction. Furthermore, we observed a reduced mitochondrial respiratory capacity and loss of redox homeostasis. Finally, we found a lower activity of enzymes related to mitochondrial fusion, these changes were accompanied by an increase in the number of small mitochondria. Once characterized mitochondrial function and dynamics, we evaluated the effect of exercise training in these variables in rats with cardiac dysfunction. The exercise training, currently established as an important non-pharmacological treatment for cardiovascular diseases, reversed the pathological cardiac remodeling and minimized the ventricular dysfunction in infarcted animals. Furthermore, exercise training restored the mitochondrial function by increasing respiratory capacity and reducing oxidative stress. Finally, exercise training restored the activity of mitochondrial dynamics-related enzymes and morphology. Taken together, our findings uncover the potential benefits of exercise training in reversing the cardiac mitochondriopathy observed in failing hearts, reinforcing the importance of this intervention as a non-pharmacological tool for heart failure therapy (AU)

FAPESP's process: 09/12349-2 - Characterization of mitochondrial function and dynamics in cardiac dysfunction-induced myocardial infarction in rats
Grantee:Juliane Cruz Campos
Support Opportunities: Scholarships in Brazil - Master