energy for elaborate cellular functions to evolve, while the organism provided the mitochondria with an environment to thrive. Today, mitochondria are found in all human cells, except for red blood cells. They take on a pivotal role in cellular fate, as they produce most of the energy (ATP) and are involved in a large number of cellular and metabolic processes. The density of the organelles is particularly high in cells requiring a lot of cellular energy - e.g. cardiomyocytes or brain cells.

Mitochondria function, and hence energy supply to the cell, may be impaired due to acute insults (e.g. ischemia) or genetic disorders (e.g. LOHN).

Researchers at Harvard University developed an approach for mitochondria augmentation and replacement to ameliorate the damages from ischemia-reperfusion injury. Ischemia is a lack of blood flow leading to an undersupply of oxygen and an impairment of mitochondria function. Reperfusion describes the re-introduction of blood flow, inducing an oversupply of oxygen. Both, ischemia and reperfusion, damage cells, with the mitochondria dysfunction being at the heart of the injury. The cascade of events, from ischemia to reperfusion, will eventually lead to cell death. The most prominent acute conditions associated with ischemia-reperfusion injury are heart attacks. At Cellvie, we are developing a means to transplant viable mitochondria into the compromised cells, to interrupt the said cascade of events, re-enabling the cells to turn oxygen into energy via the mitochondria.