Mitochondria play a key role in the homeostasis of the vast majority of the body’s cells. In the myocardium, mitochondria constitute 30% of the total myocardial cell volume. Temporary attenuation or obstruction of blood flow to the myocardium inhibits oxygen delivery to myocardial cells (ischemia), severely altering mitochondrial structure and function. These alterations in mitochondrial structure and function occur during ischemia and continue after blood flow and oxygen delivery to the myocardium is restored, and significantly decrease myocardial contractile function and myocardial cell survival.
Replacement of mitochondria damaged by ischemia would provide a mechanism to enhance cellular function and cellular rescue following the restoration of blood flow. The transplantation of autologous mitochondria, isolated from the patient’s own body directly injected into the myocardial during early reperfusion to augment the function of native mitochondria damaged during ischemia enhances myocardial post-ischemic functional recovery and cellular viability. Once internalized the transplanted mitochondria rescue cellular function and replace damaged mitochondrial DNA. There is no immune or auto-immune reaction and there is no pro-arrhythmia as a result of the transplanted mitochondria. Mitochondrial transplantation can be effective in a number of cell types and diseases. These include cardiac and skeletal muscle, pulmonary and hepatic tissue and cells and in neuronal tissue.
We provide a methodology for the isolation of mitochondria and we have an FDA approved methodology for the uptake and internalization of mitochondria. We envision that mitochondrial transplantation will be a valued treatment for all clinicians and surgeons for the treatment of varied ischemic disorders, mitochondrial diseases and overall important tool for tissue regeneration.