朱玲新

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Personal Information

Supervisor of Master's Candidates

Supervisor of Doctorate Candidates

  • E-Mail:

  • School/Department:

    口腔医学院

  • Administrative Position:

    科研办公室主任

  • Education Level:

    With Certificate of Graduation for Doctorate Study

  • Business Address:

    武汉大学口腔医学院

  • Gender:

    Male

  • Contact Information:

    lingxin.zhu@whu.edu.cn

  • Professional Title:

    Chief physician

  • Status:

    Employed

  • Academic Titles:

    中华口腔医学会口腔医学教育专委会常务委员、中国病理生理学会内分泌与代谢专委会委员、中国医院协会模拟医学专委会委员

  • Other Post:

    美国密西根大学客座副教授

  • Alma Mater:

    武汉大学

    • Discipline:

    Clinical Stomatology

Other Contact Information

  • ZipCode:

  • PostalAddress:

  • Email:

Paper Publications

Current position: Home > Scientific Research > Paper Publications

STAT3/mitophagy axis coordinates macrophage NLRP3 inflammasome activation and inflammatory bone loss

  • Date:2024-10-26  Hits:Times

  • DOI number:  

    10.1002/jbmr.4756

  • Journal:  

    J Bone Miner Res

  • Abstract:  

    Signal transducer and activator of transcription 3 (STAT3), a cytokine-responsive transcription factor, is known to play a role in immunity and bone remodeling. However, whether and how STAT3 impacts macrophage NLR family pyrin domain containing 3 (NLRP3) inflammasome activation associated with inflammatory bone loss remains unknown. Here, STAT3 signaling is hyperactivated in macrophages in the context of both non-sterile and sterile inflammatory osteolysis, and this was highly correlated with the cleaved interleukin-1 beta (IL-1 beta) expression pattern. Strikingly, pharmacological inhibition of STAT3 markedly blocks macrophage NLRP3 inflammasome activation in vitro, thereby relieving inflammatory macrophage-amplified osteoclast formation and bone-resorptive activity. Mechanistically, STAT3 inhibition in macrophages triggers PTEN-induced kinase 1 (PINK1)-dependent mitophagy that eliminates dysfunctional mitochondria, reverses mitochondrial membrane potential collapse, and inhibits mitochondrial reactive oxygen species release, thus inactivating the NLRP3 inflammasome. In vivo, STAT3 inhibition effectively protects mice from both infection-induced periapical lesions and aseptic titanium particle-mediated calvarial bone erosion with potent induction of PINK1 and downregulation of inflammasome activation, macrophage infiltration, and osteoclast formation. This study reveals the regulatory role of the STAT3/mitophagy axis at the osteo-immune interface and highlights a potential therapeutic intervention to prevent inflammatory bone loss. (c) 2022 American Society for Bone and Mineral Research (ASBMR).

  • Co-author:  

    Sun X, Yu J, Li T, Zhao H, Ji Y

  • Indexed by:  

    Journal paper

  • Correspondence Author:  

    Peng B, Du M

  • Volume:  

    38

  • Issue:  

    2

  • Page Number:  

    335-353

  • Translation or Not:  

    no

  • Date of Publication:  

    2023-02-25

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