A controlled in vitro model of disuse atrophy reveals that skeletal muscle drives its own wasting via extracellular vesicles
We established a controlled in vitro model of muscle disuse using simulated microgravity, eliminating systemic influences. This model accurately recapitulates transcriptional and proteomic signatures of inactive muscles in vivo. We discovered that extracellular vesicles (EVs) secreted by unloaded myotubes induce catabolic signaling in recipient muscle cells. Our findings reveal that skeletal muscle can drive its own disuse atrophy through EV-mediated communication.
