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Related Experiment Video

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Less-Invasive Technique for Non-stabilized Mandibular Fracture in Mouse Models
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Mechanosensitive Piezo1/Osteocalcin/Irisin Axis Protects Against Disuse-Induced Muscle Atrophy.

Zhaolu Wang1, Xiuying Jiang1, Xi Sun1

  • 1College of Animal Science and Technology, Northwest A&F University, Yangling, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|April 17, 2026
PubMed
Summary

A newly discovered Piezo1/osteocalcin/Irisin pathway links bone health to muscle mass. This axis protects against disuse muscle atrophy, offering a potential therapeutic target for conditions like immobilization.

Keywords:
Fndc5/IrisinPiezo1muscle atrophyosteocalcin

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Area of Science:

  • Biochemistry
  • Physiology
  • Molecular Biology

Background:

  • Disuse-induced muscle atrophy is a significant clinical problem.
  • The role of bone-derived hormones, like osteocalcin (OCN), in muscle atrophy is not well understood.

Purpose of the Study:

  • To investigate the role of osteocalcin (OCN) in disuse muscle atrophy.
  • To identify the molecular mechanisms linking bone mechanotransduction to muscle homeostasis.

Main Methods:

  • Bilateral hindlimb immobilization (IMM) in animal models.
  • Assessment of OCN levels and muscle mass.
  • Pharmacological activation and genetic knockdown of Piezo1.
  • Analysis of OCN receptor Gprc6a and downstream Fndc5/Irisin.

Main Results:

  • IMM reduced circulating OCN, and OCN deficiency worsened atrophy.
  • Exogenous OCN attenuated muscle atrophy and promoted recovery.
  • The Piezo1/OCN/Irisin axis was identified as a key regulator.
  • OCN's protective effects were independent of food intake and conserved in porcine myotubes.

Conclusions:

  • The Piezo1/Osteocalcin/Irisin axis is crucial for maintaining muscle homeostasis during mechanical unloading.
  • This axis represents a promising therapeutic target for disuse-induced muscle atrophy.