Mitochondria Transplantation May Improves Recovery after Cardiac Arrest
Mitochondria are organelles that act as the food-processing center of our cells. Recently, the team from the Feinstein Institutes for Medical Research has shown that mitochondria transplantation (MTx), the approach of delivering fresh mitochondria to critical tissues, can improve survival and neurological outcomes after cardiac arrest.
Cardiac arrest is a life-threatening condition where a heart stops beating, the blood flow stops subsequently and the delivery of oxygen to the brain and other vital organs is blocked. This lethal condition of hypoxia will cause severe brain injury, but the quicker the heart can be restarted, the better prognosis will be expected.
With the current approach, the overall survival of rats improved and the repair of the ischemic brain was accelerated according to the study published in the journal BMC Medicine.
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The Role of Mitochondria in Body Cells
Mitochondria are special organelles that have the ability to generate ATP with aerobic respiration, which requires oxygen, that’s why our cells need oxygen deliveries from blood. When oxygen delivery stops, mitochondria can no longer produce energy, and soon the cell is in danger of dying. Our brain, which controls fundamental parts of our body functions, is one of the organs which requires the most oxygen supply.
There is some past evidence showing mitochondria are able to assist in the repair of other mitochondria, for example, injured mitochondria are still capable of self-repair and cellular protection through fission, fusion, and mitophagy. The mechanisms of intercellular mitochondrial transfer were also shown to have protective effects in muscular tissues.
A Novel Approach to Reverse Cells Damage
Thus, in this present study, the research team decided to test the effectiveness of transplantation in a cardiac arrest event with a specific focus on neuronal tissue health. The researchers first confirmed that donor mitochondria can be taken up by neurons growing in culture before attempting to transfer mitochondria into murine models.
Mitochondria extracted from rat brain and muscle tissues were stained red and mitochondria of the neural cells were stained green. The donated mitochondria were taken up into cultured neural cells and co-localized with endogenous mitochondria inside neural cells. The in vivo test is then started after success in the cell model.
As a result, the 72-hour survival rate was 91% in freshly isolated mitochondria transplantation compared to just 55% in the negative control. Improvements in rapid recovery of arterial lactate, glucose levels, cerebral microcirculation, neurological function, and decreased lung injury were observed with improved survival rates. More importantly, as the frozen-thawed mitochondria did not have a protective effect, the mitochondrial activity from the fresh samples seems to be the key to the protective effect.
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