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Characterization of mitochondrial function and dynamics in cardiac dysfunction-induced myocardial infarction in rats

Grant number: 09/12349-2
Support type:Scholarships in Brazil - Master
Effective date (Start): March 01, 2010
Effective date (End): February 29, 2012
Field of knowledge:Biological Sciences - Physiology
Principal Investigator:Julio Cesar Batista Ferreira
Grantee:Juliane Cruz Campos
Home Institution: Escola de Educação Física e Esporte (EEFE). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

Myocardial infarction is currently considered the etiology that most contributes to the onset of heart failure (HF) in humans. The progression of cardiac dysfunction due to the myocardium injury is accompanied by a number of metabolic changes that result in energy deficits and reprogramming of cell signaling. Representing approximately one-third of cardiac mass, mitochondria play a critical role in energy metabolism. Disruption of mitochondrial metabolism, such as reduced oxygen consumption and exacerbated production of free radicals, are associated with worsening of cardiac dysfunction and the onset of HF. Currently, little is known about the contribution of mitochondrial fusion and fission processes in cardiac dysfunction, as well as its interaction with mitochondrial metabolism. Therefore, in order to better understand the cellular mechanisms involved in the reorganization of mitochondrial biology during cardiac dysfunction, we propose in this project a better characterization of mitochondrial function and dynamics in animal model of cardiac dysfunction induced by myocardial infarction. Detailed understanding of mitochondrial function and dynamics will be of great value for future use of therapies to reverse the mitochondriopathy usually present in the pathophysiology of cardiovascular diseases.

Matéria(s) publicada(s) na Agência FAPESP sobre a bolsa:
Research reveals how physical exercise protects the heart 
Physical exercise helps prevent the worsening of heart failure 

Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
FERREIRA, JULIO C. B.; CAMPOS, JULIANE C.; QVIT, NIR; QI, XIN; BOZI, LUIZ H. M.; BECHARA, LUIZ R. G.; LIMA, VANESSA M.; QUELICONI, BRUNO B.; DISATNIK, MARIE-HELENE; DOURADO, PAULO M. M.; KOWALTOWSKI, ALICIA J.; MOCHLY-ROSEN, DARIA. A selective inhibitor of mitofusin 1-beta IIPKC association improves heart failure outcome in rats. NATURE COMMUNICATIONS, v. 10, JAN 18 2019. Web of Science Citations: 4.
CAMPOS, JULIANE C.; QUELICONI, BRUNO B.; BOZI, LUIZ H. M.; BECHARA, LUIZ R. G.; DOURADO, PAULO M. M.; ANDRES, ALLEN M.; JANNIG, PAULO R.; GOMES, KATIA M. S.; ZAMBELLI, VANESSA O.; ROCHA-RESENDE, CIBELE; GUATIMOSIM, SILVIA; BRUM, PATRICIA C.; MOCHLY-ROSEN, DARIA; GOTTLIEB, ROBERTA A.; KOWALTOWSKI, ALICIA J.; FERREIRA, JULIO C. B. Exercise reestablishes autophagic flux and mitochondrial quality control in heart failure. AUTOPHAGY, v. 13, n. 8, p. 1304-1317, 2017. Web of Science Citations: 18.
CAMPOS, JULIANE C.; QUELICONI, BRUNO B.; DOURADO, PAULO M. M.; CUNHA, TELMA F.; ZAMBELLI, VANESSA O.; BECHARA, LUIZ R. G.; KOWALTOWSKI, ALICIA J.; BRUM, PATRICIA C.; MOCHLY-ROSEN, DARIA; FERREIRA, JULIO C. B. Exercise Training Restores Cardiac Protein Quality Control in Heart Failure. PLoS One, v. 7, n. 12 DEC 27 2012. Web of Science Citations: 44.

Please report errors in scientific publications list by writing to: cdi@fapesp.br.