Deficient early canonical BMP9-SMAD signaling and dysregulated macrophage microenvironment characterize the failure of bone healing in a critical-size defect model - Takeaways - MDSpire

Impaired Early BMP9-SMAD Pathway and Altered Macrophage Environment Contribute to Bone Healing Deficits in a Critical-Size Defect Model

  • By

  • Kai Zhong

  • Yufei Shao

  • Yu Zhou

  • Zengyi Huang

  • Xing Liu

  • July 20, 2026

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  • 1

    Atrophic non-union is characterized by impaired inflammation resolution and delayed osteogenesis, posing significant clinical challenges.

  • 2

    A critical window of 1-2 weeks post-fracture shows significant inhibition of BMP9-SMAD signaling in the non-union microenvironment.

  • 3

    Sustained accumulation of M1 macrophages and impaired M2 polarization contribute to bone healing deficits in critical-size defects.

  • 4

    BMP9 promotes M2 macrophage polarization and inhibits osteoclastogenesis through the canonical SMAD-ID1 pathway.

  • 5

    Disruption of BMP9-SMAD signaling leads to an imbalance in immune cell recruitment and bone remodeling, contributing to atrophic non-union.

Original Source(s)

Deficient early canonical BMP9-SMAD signaling and dysregulated macrophage microenvironment characterize the failure of bone healing in a critical-size defect model

  • by Kai Zhong, Yufei Shao, Yu Zhou, Zengyi Huang, Xing Liu

  • July 20, 2026

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