Autophagy plays a beneficial role against mitochondrial dysfunction in cardiomyocytes

Healthy mitochondria are vital for cellular homeostasis and survival. Oxidatively stressed mitochondria can release pro-apoptotic signals causing cell death. Dysfunctional mitochondria are removed by autophagy, a process during which damaged proteins and organelles are sequestered and degraded. ObjectiveTo determine whether interventions targeted to upregulate autophagy can protect HL-1 cardiomyocytes against enhanced mitochondrial damage in HL-1 cardiomyocytes. MethodsHL-1 cells were treated with the mitochondrial toxin Antimycin A (AMA), and mitochondrial superoxide generation, membrane potential, cellular DNA/RNA oxidation and cell viability were determined. Autophagy was stimulated using amino acid starvation or Rapamycin, and monitored with immunoblotting and epifluorescence imaging. Cell viability was tested with the MTT assay. ResultsAMA increased mitochondrial superoxide generation, decreased membrane potential, increased cellular DNA/RNA oxidation and decreased cell viability of HL-1 cells. Both ...