Fig. 5

The cellular and molecular mechanisms of mitochondrial transfer. Mitochondrial transfer can be triggered by various intracellular and extracellular signals in recipient cells, including hypoxia, oxidative stress and inflammation, and the latter can recruit donor cells to induce mitochondrial ejection. Damaged mitochondria in recipient cells may elicit danger signals to induce mitochondrial transfer from donor cells, act as DAMPs and induce the expression of HO-1 and mitochondrial biogenesis in MSCs, increasing mitochondrial transfer and restoring MSC function to damaged cells. CECs were pretreated with rotenone to induce ROS production, resulting in the expression of M-Sec through the activation of NF-κB, which contributed to the formation of TNTs in CECs and increased mitochondrial transfer from MSCs to CECs. Both Sig-1R and calcium ions modulate mitochondrial transfer. During the process of mitochondrial transfer, Miro proteins directly bind to the kinesin motor protein KIF5 in conjunction with accessory proteins such as TRAK1, TRAK2, MYO10, and MYO19, forming a motor‒adaptor complex that facilitates the mobility of mitochondria along microtubules