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.
News published in Agência FAPESP Newsletter about the scholarship: