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p21 induces a senescence program and skeletal muscle dysfunction.

Davis A Englund1, Alyssa Jolliffe1, Zaira Aversa1

  • 1Robert and Arlene Kogod Center on Aging, Mayo Clinic, Rochester, MN, USA; Department of Physical Medicine and Rehabilitation, Mayo Clinic, Rochester, MN, USA.

Molecular Metabolism
|December 12, 2022
PubMed
Summary
This summary is machine-generated.

Elevated p21 protein triggers cellular senescence and muscle problems. This study shows p21 alone causes skeletal muscle atrophy, fibrosis, and dysfunction, revealing a new cause of muscle loss.

Keywords:
AgingCellular senescenceDNA damageFibrosisPhysical functionSarcopeniaSenescence-associated secretory phenotype

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Area of Science:

  • Cellular Biology
  • Muscle Physiology
  • Aging Research

Background:

  • Elevated p21 levels correlate with senescent cell accumulation and skeletal muscle dysfunction in both mice and humans.
  • The precise mechanistic role of p21 in driving skeletal muscle pathology remains to be fully elucidated.

Purpose of the Study:

  • To investigate whether p21 overexpression is sufficient to induce cellular senescence and pathological features in skeletal muscle.
  • To explore the mechanistic contribution of p21 to skeletal muscle dysfunction.

Main Methods:

  • Utilized a mouse model with p21 overexpression (p21OE).
  • Assessed core properties of cellular senescence, including transcriptomic changes, DNA damage, and mitochondrial function.
  • Evaluated the senescence-associated secretory phenotype (SASP).
  • Compared pathological features (atrophy, fibrosis) and physical function in p21OE mice versus age-matched controls.

Main Results:

  • p21 overexpression induced key features of cellular senescence in skeletal muscle.
  • Observed altered transcriptome, DNA damage, and mitochondrial dysfunction in p21OE muscle.
  • Confirmed the induction of SASP by p21.
  • p21OE mice displayed significant skeletal muscle atrophy, fibrosis, and impaired physical function compared to controls.

Conclusions:

  • p21 is sufficient to drive a cellular senescence program in skeletal muscle.
  • p21 overexpression directly contributes to skeletal muscle atrophy, fibrosis, and functional decline.
  • These findings identify p21 as a novel factor implicated in age-related skeletal muscle loss and dysfunction.