Jalal Pourahmad - Department of Pharmacology and Toxicology, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Abdollah Armjand - Department of Pharmacology and Toxicology, School of Pharmacy, Shahid Beheshti University of Medical Sciences, Tehran, Iran

Previously, it was demonstrated that the transplantation of viable, structurally intact, respiration competent mitochondria into the ischemic myocardium during early reperfusion significantly enhanced cardioprotection by decreasing myocellular damage and enhancing functional recovery. Our in vitro and in vivo studies established that autologous mitochondria are internalized into cardiomyocytes, liver hepatocytes andrenalproximal tubular cells.Following transplantation; however, the mechanism(s) modulating internalization of these organelles were poorly understood. It was shown that internalization of mitochondria occurs through actin-dependent endocytosis and rescues cell function by increasing ATP content and oxygen consumption rates. It was also proven that internalized mitochondria replace depleted mitochondrial (mt)DNA. The previously published work describe the mechanism for internalization of mitochondria within host cells and provide a basis for novel therapeutic interventions allowing for the rescue and replacement of damaged or impaired mitochondria.

Mitochondria, Transplantation, Cardioprotection, Mitochondrial DNA, Endocytosis