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  1. Home
  3. Ncoa4-mediated Ferritinophagy Promotes Pyroptosis By Reactive Oxygen Species Generation In The Progress Of Gingival Inflammation.
  1. Home
  3. Ncoa4-mediated Ferritinophagy Promotes Pyroptosis By Reactive Oxygen Species Generation In The Progress Of Gingival Inflammation.

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NCOA4-mediated ferritinophagy promotes pyroptosis by reactive oxygen species generation in the progress of gingival

Xinyi Ren1, Zhilong Huang2, Miaomiao Han2

  • 1Nanjing Stomatological Hospital, Affiliated Hospital of Medical School, Research Institute of Stomatology, Nanjing University, Nanjing, China.

Cellular Signalling
|June 11, 2025

View abstract on PubMed

Summary
This summary is machine-generated.

Nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy increases iron and reactive oxygen species (ROS), promoting pyroptosis in inflamed tissues. Targeting iron homeostasis via ferritinophagy may offer new therapeutic strategies for inflammatory diseases.

Keywords:
FerritinophagyGingivitisInflammationPyroptosisROS

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Area of Science:

  • Cellular Biology
  • Immunology
  • Pathology

Background:

  • Intracellular iron imbalance can lead to excessive reactive oxygen species (ROS) via Fenton reactions.
  • Nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy contributes to iron and ROS accumulation.
  • The link between ferritinophagy-induced iron generation and pyroptosis remains unclear.

Purpose of the Study:

  • To investigate whether ferritinophagy-mediated endogenous iron generation exacerbates pyroptosis.
  • To explore the role of NCOA4-mediated ferritinophagy in inflamed gingival tissues and lipopolysaccharide (LPS)-treated macrophages.

Main Methods:

  • Activation of NCOA4-mediated ferritinophagy was observed in inflamed gingival tissues and LPS-treated macrophages.
  • Elevated iron levels were found to promote pyroptosis through caspase-1-gasdermin D (GSDMD) and caspase-3-gasdermin E (GSDME) pathways in a ROS-dependent manner.
  • Iron chelation was used to assess its effect on LPS and ferrous iron-induced pyroptosis and inflammation.

    • Main Results:

    • NCOA4-mediated ferritinophagy was activated in inflamed gingival tissues and LPS-treated macrophages.
    • Elevated iron levels promoted pyroptosis via ROS-dependent caspase-1/GSDMD and caspase-3/GSDME pathways.
    • Iron chelation reduced inflammatory cytokine release and pyroptosis in macrophages and inflamed gingival tissues.

    Conclusions:

    • NCOA4-mediated ferritinophagy promotes pyroptosis in inflamed gingival tissues.
    • This study highlights a novel connection between iron homeostasis, ferritinophagy, and pyroptosis.
    • Targeting ferritinophagy or its downstream effects on pyroptosis presents a potential therapeutic avenue for inflammatory diseases.