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

Fecha de publicación: 15/10/2021 Fecha Ahead of Print: 14/10/2021

Autores de INCLIVA

• Esther Garcia Dominguez

  Autor

• 

  Maria Carmen Gomez Cabrera

  Autor

Participantes ajenos a INCLIVA

• Roman, William
• Pinheiro, Helena
• Pimentel, Mafalda R
• Segales, Jessica
• Oliveira, Luis M
• Serrano, Antonio L
• Gomes, Edgar R
• Munoz-Canoves, Pura

Grupos y Plataformas de I+D+i

• Grupo de Investigación en Ejercicio, Nutrición y Estilo de Vida Saludable

  

  Established Researcher

  Maria Carmen Gomez Cabrera

Abstract

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.