Heart is known as an organ with limited regenerative capacity, that faced with an injury, such as myocardial infarction, undergoes repair by non-contractile fibrous tissue and progresses to heart failure. Recent evidences has demonstrated replacement of cardiac cells over the years in mammals, especially in human, however, these rates are still low about 0.5 to 2%/year. Was also recently demonstrated the complete cardiac regeneration in neonatal mice with 1 day of age who underwent partial resection of the heart, which opened a precedent for studies on the maintenance of the regenerative capacity of postnatal heart. In our laboratory, preliminary studies show that the same regeneration occurs in rat. This period in which the cardiac regeneration occurs in newborn mice corresponds to the period in which the changes of energy metabolism, due specialization of cardiac cells and increased energy demands, and we can still detect proliferation of cardiomyocytes, which shows a close relationship between cardiomyogenese and mitochondrial biogenesis. Understanding the molecular mechanisms that regulate endogenous cell cycle and mitochondrial energy metabolism of cardiomyocytes could reveal important clues about how to stimulated cardiomyogenese in adults. In this sense, the model of heart regeneration in rats with the using the technique of MALDI Imaging will assistin obtaing differential patterns of protein expression in hearts of progress of apical cardiac regeneration after resection. These data may reveal how mitochondrial energy metabolism could influence and determine cardiac regeneration and mobilization of endogenous cardiac repair mechanisms in adults.
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