Muscle repair after physiological damage relies on nuclear migration for cellular reconstruction

Regeneration of skeletal muscle is a highly synchronized process that requires muscle stem cells (satellite cells). We found that localized injuries, as experienced through exercise, activate a myofiber self-repair mechanism that is independent of satellite cells in mice and humans. Mouse muscle injury triggers a signaling cascade involving calcium, Cdc42, and phosphokinase C that attracts myonuclei to the damaged site via microtubules and dynein. These nuclear movements accelerate sarcomere repair and locally deliver messenger RNA (mRNA) for cellular reconstruction. Myofiber self-repair is a cell-autonomous protective mechanism and represents an alternative model for understanding the restoration of muscle architecture in health and disease.

Automated summary

The study revealed that localized muscle injuries triggered by exercise activate a myofiber self-repair mechanism that is independent of satellite cells. A signaling cascade involving calcium, Cdc42, and phosphokinase C attracts myonuclei to the damaged site, accelerating sarcomere repair and delivering messenger RNA for cellular reconstruction. Myofiber self-repair is a cell-autonomous protective mechanism, offering an alternative model for understanding muscle architecture restoration in health and disease.