Senescence as a regulatory mechanism in skeletal muscle repair in young mice
Abstract
Senolytic treatment in young mice results in a transient delay in the repair kinetics of satellite cells, macrophages, and fibrosis without disrupting functional repair of skeletal muscle. Fibers associated with a p21+ nucleus were smaller in size than myofibers not associated with a p21+ nucleus, possibly signifying areas with delayed or incomplete repair or where greater senescence-associated signalling is needed to regulate nearby cell populations.
Fields of Study & Subjects
Telomeres
Telomerase
and Senescence
Muscle Physiology and Disorders
Mesenchymal stem cell research
Publication details
- Journal / source
- American Journal of Physiology-Cell Physiology
- Publisher
- American Physiological Society
- Volume
- 331
- Issue
- 2
- Pages
- C316–C327
- Publication date
- 18 June 2026
- Language
- EN