Principal Investigator: Dr Jelena Begovic
Autophagy presents an adaptive response to unfavorable conditions and mediates highly regulated self-eating process via lysosomes. Autophagy is induced by deprivation of nutrients, hormones, and energy. Autophagy undertakes cytoprotective function through the modulation of cell viability (cell attempt to survive) or might play important role in cell death as a part of the process of apoptosis. Autophagy involves degradation and recycling of cytoplasmatic components, including long-lived proteins and organelles, thus maintaining cellular energy homeostasis. Current evidence suggests that autophagy can selectively remove damaged organelles such as the mitochondria. Mitochondria-induced oxidative stress has been shown to play a major role in a wide range of pathologies in several organs, including the heart. Moreover, in advanced stages of heart failure, ATP production from energy-providing substrates is impaired. One source of amino acids that can sustain the failing heart is the degradation of intracellular proteins via autophagy.