Membrane nanotubes (MNTs) act as "highways" between cells to facilitate the 
transfer of multiple signals and play an important role in many diseases. Our 
previous work reported on the transfer of mitochondria via MNTs between 
cardiomyocytes (CMs) and cardiac myofibroblasts (MFs); however, the elucidation 
of the underlying mechanism and pathophysiological significance of this transfer 
requires additional study. In this study, we determined that the mean movement 
velocity of mitochondria in MNTs between CMs and MFs was approximately 
17.5 ± 2.1 nm/s. Meanwhile, treatment with microtubule polymerisation inhibitors 
nocodazole or colcemid in cell culture decreased mitochondrial velocity, and 
knockdown of the microtubule motor protein kinesin family member 5B (KIF5B) led 
to a similar effect, indicating that mitochondrial movement was dependent on 
microtubules and the motor protein KIF5B. Furthermore, we showed that 
hypoxia/reoxygenation-induced CM apoptosis was attenuated by coculture with 
intact or hypoxia/reoxygenation-treated MFs, which transferred mitochondria to 
CMs. This rescue was prevented either by separating the cells using Transwell 
culture or by impairing mitochondrial transfer with nocodazole or colcemid 
treatment. In conclusion, as a novel means of intercellular communication, MNTs 
rescue distressed CMs from apoptosis by transporting mitochondria along 
microtubules via KIF5B.