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Related Experiment Video

Updated: Jan 11, 2026

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Microvascular Endothelial Cell-Derived Exosomes Decrease Osteoclastogenesis by Restraining Osteoclast Ferroptosis

Yajun Liu1, Chen Xu1, Zhaodong Wang1

  • 1Department of Orthopedics, The First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, China; and Anhui Province Key Laboratory of Tissue Transplantation, Bengbu Medical University, Bengbu, Anhui, China.

Critical Reviews in Immunology
|November 10, 2025
PubMed
Summary

Skeletal muscle microvascular endothelial cell-derived exosomes carrying USP13 inhibit osteoclast formation and ferroptosis. This finding offers a potential therapeutic strategy for osteolytic diseases by targeting exosomal USP13.

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Orthopedics

Background:

  • Exosomes (EXOs) modulate ferroptosis in orthopedic conditions.
  • The role of EXOs in osteoclast function and ferroptosis is not well understood.

Purpose of the Study:

  • To investigate the effects of MMECs-derived EXOs on osteoclastogenesis and ferroptosis.
  • To elucidate the underlying mechanisms involving USP13.

Main Methods:

  • EXOs were isolated from MMECs.
  • Osteoclasts were generated from RAW264.7 cells stimulated with RANKL.
  • Effects of EXOs and USP13 on osteoclastogenesis and ferroptosis were assessed.
  • USP13 expression and NRF2/GPX4 pathway activation were analyzed.

Main Results:

  • EXO treatment reduced osteoclast formation and expression of osteoclast-specific genes.
  • EXOs counteracted RANKL-induced ferroptosis markers (increased ferrous iron, MDA, LDH, ROS; decreased NRF2, GPX4).
  • USP13, carried by EXOs, suppressed osteoclastogenesis and ferroptosis, activating the NRF2/GPX4 pathway.

Conclusions:

  • MMECs-derived exosomal USP13 demonstrates anti-osteoclastogenesis effects by regulating ferroptosis.
  • USP13 delivered via exosomes presents a potential therapeutic target for osteolytic diseases.