Mitochondrial transfer between cells can rescue aerobic respiration. This study demonstrates that functional mitochondria or mtDNA can be transferred from adult stem cells or somatic cells to rescue aerobic respiration in mammalian cells with nonfunctional mitochondria. The research used A549 ρ° cells, which have nonfunctional mitochondria and cannot perform aerobic respiration. When these cells were cocultured with human bone marrow-derived stem/progenitor cells (hMSCs) or skin fibroblasts, they were able to rescue aerobic respiration. The rescued cells showed functional mitochondria, increased ATP production, reduced lactate production, lower reactive oxygen species, increased membrane potential, and higher oxygen consumption. Genetic analysis confirmed that the rescued cells contained mtDNA from the donor cells, indicating mitochondrial transfer without cell fusion. The study also showed that mitochondria can actively transfer between cells, with hMSCs directing cytoplasm toward A549 ρ° cells and mitochondria streaming through cytoplasmic extensions. The results suggest that mitochondrial transfer is an active cellular process, not passive uptake. The findings have implications for treating mitochondrial diseases, as functional mitochondria can be transferred from healthy cells to rescue cells with defective mitochondria. The study also highlights the potential of hMSCs and other progenitor cells in treating diseases such as spinal cord injury, stroke, and heart disease.Mitochondrial transfer between cells can rescue aerobic respiration. This study demonstrates that functional mitochondria or mtDNA can be transferred from adult stem cells or somatic cells to rescue aerobic respiration in mammalian cells with nonfunctional mitochondria. The research used A549 ρ° cells, which have nonfunctional mitochondria and cannot perform aerobic respiration. When these cells were cocultured with human bone marrow-derived stem/progenitor cells (hMSCs) or skin fibroblasts, they were able to rescue aerobic respiration. The rescued cells showed functional mitochondria, increased ATP production, reduced lactate production, lower reactive oxygen species, increased membrane potential, and higher oxygen consumption. Genetic analysis confirmed that the rescued cells contained mtDNA from the donor cells, indicating mitochondrial transfer without cell fusion. The study also showed that mitochondria can actively transfer between cells, with hMSCs directing cytoplasm toward A549 ρ° cells and mitochondria streaming through cytoplasmic extensions. The results suggest that mitochondrial transfer is an active cellular process, not passive uptake. The findings have implications for treating mitochondrial diseases, as functional mitochondria can be transferred from healthy cells to rescue cells with defective mitochondria. The study also highlights the potential of hMSCs and other progenitor cells in treating diseases such as spinal cord injury, stroke, and heart disease.