Eliminating Elevated p53 Signaling Fails to Rescue Skeletal Muscle Defects or Extend Survival in Lamin A/C-Deficient Mice

Using three laminopathy models, researchers found that increased p53 activity in Lmna-mutant muscle cells primarily resulted from mechanically induced damage to the myonuclei, and not from altered transcriptional regulation due to loss of lamin A/C expression.