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Transfer of mitochondria to injured cells is a unique phenomenon whereby healthy donor cells, such as mesenchymal stem cells, deliver functional mitochondria to recipient injured cells. This process primarily occurs via cellular structures like tunneling nanotubes, vesicles, or cell fusion and is central to the regenerative effects of stem cell-based therapies. Mitochondrial transfer can rescue damaged cells from energy deficit, reduce apoptosis, restore antioxidant defenses, and promote tissue repair. Recent research has identified molecular mediators, such as connexin-43 and Miro1, that regulate the transfer efficiency. Although not a direct molecular target, this process has therapeutic implications for diseases such as cardiovascular disease, inflammation, neurodegeneration, diabetic complications, and even cancer, though there are concerns about safety and specificity as well as potential risks if the process is hijacked by tumor cells.
Stem cell therapeutics facilitate mitochondrial transfer by tunneling nanotubes (TNTs), extracellular vesicles (EVs), gap junctions, microvesicles, cell fusion, and related mechanisms. Overexpression of proteins like Miro1 increases transfer efficiency. Restoration of recipient cell mitochondria via fusion, fission, reduction of oxidative stress, and upregulation of antioxidant defense.
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