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Rethinking Muscle Aging Through the Lens of Fibro-Adipogenic Progenitors.

Feng-Min Zhang1, Xian-Zhong Zhang1, Zhen Yu1

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|November 10, 2025
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Summary
This summary is machine-generated.

Aging muscle develops fibrosis and fat due to fibro-adipogenic progenitors (FAPs). Understanding FAP reprogramming in aged muscle is key to restoring muscle function and combating sarcopenia.

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Area of Science:

  • Muscle biology
  • Aging research
  • Cellular and molecular mechanisms of aging

Background:

  • Skeletal muscle aging involves interstitial adipose and fibrotic tissue deposition, impairing structure and function.
  • This maladaptive remodeling compromises muscle performance, regenerative capacity, and contributes to frailty and sarcopenia.
  • Fibro-adipogenic progenitors (FAPs) are the primary cellular source of pathological fibrosis and adipogenesis in muscle.

Purpose of the Study:

  • To summarize current knowledge on the roles and dynamics of FAPs in aged muscle.
  • To discuss FAPs as potential therapeutic targets for rejuvenating aged muscle.
  • To understand how aging reprograms FAP fate and function for muscle regeneration.

Main Methods:

  • Review of current scientific literature on FAPs in muscle aging.
  • Analysis of cellular and molecular mechanisms driving FAP dysfunction.
  • Exploration of therapeutic strategies targeting FAPs for muscle rejuvenation.

Main Results:

  • In young muscle, FAPs transiently support regeneration; in aged muscle, they promote fibrosis and fat accumulation.
  • Aged muscle niches exhibit chronic inflammation, altered matrix, and impaired communication, driving FAP maladaptation.
  • FAP dysfunction is a central mechanism in age-related sarcopenia, injury susceptibility, and delayed recovery.

Conclusions:

  • Dysfunctional FAPs contribute significantly to age-related muscle decline and sarcopenia.
  • Targeting FAP reprogramming offers a promising strategy to restore muscle regenerative capacity.
  • Rejuvenating the aged muscle niche by modulating FAPs could mitigate muscle aging effects.