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Updated: Jun 11, 2026

Ferritinophagy: Assessing the Selective Degradation of Iron by Autophagy in Human Fibroblasts
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JAK/STAT signaling as a key regulator of ferroptosis: mechanisms and therapeutic potentials in cancer and diseases.

Yimeng Dai1, Chunguo Cui2, Dan Jiao3

  • 1Department of Radiology, China-Japan Union Hospital, Jilin University, Changchun, China.

Cancer Cell International
|March 7, 2025
PubMed
Summary

Ferroptosis, a cell death process, is regulated by the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. This pathway can either promote or inhibit ferroptosis, offering therapeutic targets for diseases like cancer and neurodegeneration.

Keywords:
FerroptosisJAK/STAT signalingJAK2STAT1STAT3STAT6Therapy

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Area of Science:

  • Cellular biology
  • Molecular mechanisms of disease
  • Signaling pathways

Background:

  • Ferroptosis is a regulated cell death form driven by iron-dependent lipid peroxidation.
  • It is crucial in diseases such as cancer, neurodegeneration, and tissue damage.
  • The Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway significantly influences biological processes.

Purpose of the Study:

  • To review the complex interplay between ferroptosis and the JAK/STAT signaling pathway.
  • To elucidate how JAK/STAT pathway dysregulation impacts ferroptosis in various diseases.
  • To explore therapeutic strategies targeting JAK/STAT to modulate ferroptosis.

Main Methods:

  • Literature review of studies on ferroptosis and JAK/STAT signaling.
  • Analysis of molecular mechanisms linking JAK/STAT components (JAK2, STAT1, STAT3, STAT6) to ferroptosis regulators (SLC7A11, GPX4, hepcidin).
  • Examination of ferroptosis modulation in disease contexts (cancer, neurodegeneration, inflammatory diseases).

Main Results:

  • JAK2 activation promotes ferroptosis by modulating SLC7A11, GPX4, ferritinophagy, and hepcidin.
  • STAT1 activation enhances ferroptosis by suppressing System Xc-, leading to glutathione depletion.
  • STAT3 and STAT6 activation inhibit ferroptosis by upregulating SLC7A11 and GPX4, offering cell protection.

Conclusions:

  • The JAK/STAT pathway's role in ferroptosis is context-dependent, with different STAT proteins exerting opposing effects.
  • Targeting the JAK/STAT pathway presents a promising therapeutic strategy for manipulating ferroptosis in cancer and other diseases.
  • Understanding this interplay is vital for developing novel treatments for ferroptosis-related conditions.