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The interaction between ferroptosis and inflammatory signaling pathways.

Yue Chen1, Ze-Min Fang1, Xin Yi2

  • 1Division of Cardiothoracic and Vascular Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.

Cell Death & Disease
|March 22, 2023
PubMed
Summary
This summary is machine-generated.

Inflammation, through key signaling pathways like JAK-STAT and NF-κB, can trigger ferroptosis, a cell death type. Targeting these inflammatory pathways offers therapeutic strategies for ferroptosis-related diseases.

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Area of Science:

  • Cell Biology
  • Immunology
  • Biochemistry

Background:

  • Ferroptosis is iron-dependent cell death marked by lipid peroxidation.
  • Inflammation is crucial for homeostasis but its dysregulation causes cell dysfunction and death.
  • Emerging evidence links inflammatory signaling pathway activation to ferroptosis induction.

Purpose of the Study:

  • To elucidate the role of five classical inflammatory signaling pathways in ferroptosis.
  • To explore the therapeutic potential of modulating these pathways for ferroptosis-related diseases.

Main Methods:

  • Review and analysis of existing literature on inflammatory pathways and ferroptosis.
  • Focus on JAK-STAT, NF-κB, inflammasome, cGAS-STING, and MAPK signaling pathways.
  • Examination of in vivo and in vitro studies demonstrating therapeutic interventions.

Main Results:

  • Activation of JAK-STAT, NF-κB, inflammasome, cGAS-STING, and MAPK pathways can induce ferroptosis.
  • These pathways regulate key aspects of iron metabolism and lipid peroxidation.
  • Numerous agents show therapeutic promise by targeting these inflammatory pathways.

Conclusions:

  • Inflammatory signaling pathways are critical regulators of ferroptosis.
  • Targeting these pathways presents a promising therapeutic avenue for managing ferroptosis and associated diseases.