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Exercise maintains bone homeostasis by promoting osteogenesis through STAT3.

Xiangru Huang1, Yanfei Zhu1, Siyuan Sun1

  • 1Center of Craniofacial Orthodontics, Department of Oral and Cranio-maxillofacial Surgery, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine; College of Stomatology, Shanghai Jiao Tong University; National Center for Stomatology; National Clinical Research Center for Oral Diseases; Shanghai Key Laboratory of Stomatology; Shanghai Research Institute of Stomatology.

International Journal of Biological Sciences
|May 8, 2023
PubMed
Summary

Exercise promotes bone health by activating Signal transducer and activator of transcription 3 (STAT3) in osteoblasts. This pathway is crucial for bone metabolism and may offer a therapeutic target for osteoporosis due to inactivity.

Keywords:
STAT3bone homeostasisexercisemechanical forcerunning wheeltail suspension

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Area of Science:

  • Bone biology
  • Mechanobiology
  • Cell signaling

Background:

  • Mechanical loading from exercise influences bone density and strength.
  • Disuse leads to bone loss, but the underlying mechanisms are not fully understood.
  • Understanding mechanotransduction in bone is key to maintaining skeletal health.

Purpose of the Study:

  • To investigate the role of Signal transducer and activator of transcription 3 (STAT3) in exercise-induced bone metabolism.
  • To elucidate the mechanism of mechanotransduction in bone.
  • To identify potential therapeutic targets for exercise-deficiency-related bone loss.

Main Methods:

  • Utilized running-wheel exercise and tail suspension models in mice.
  • Employed in vitro mechanical tension loading on bone marrow mesenchymal stem cells (BMSCs).
  • Used pharmacological inhibitors/agonists and conditional knockout mice to assess STAT3 function.

Main Results:

  • Mechanical loading and exercise increased osteoblastic STAT3 activity.
  • STAT3 activation promoted osteoblastic differentiation of BMSCs.
  • Inhibition or deletion of STAT3 in osteoblasts impaired exercise-induced bone gain and osteogenesis.
  • STAT3 agonist colivelin promoted osteogenesis and rescued disuse bone loss.

Conclusions:

  • Osteoblastic STAT3 is essential for exercise-mediated bone metabolism and homeostasis.
  • STAT3 signaling is a critical mediator of mechanical loading effects on bone.
  • Targeting STAT3 may offer a novel therapeutic strategy for osteoporosis resulting from inactivity.