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Ferroptosis and endoplasmic reticulum stress in rheumatoid arthritis

Qin Ao1,2, Huan Hu3, Ying Huang1,2

  • 1Guizhou Universisity of Traditional Chinese Medicine, Guiyang, China.

Frontiers in Immunology
|July 30, 2024
PubMed

Insights

Ferroptosis and endoplasmic reticulum stress (ERS) are implicated in rheumatoid arthritis (RA). This review explores their potential correlation, offering insights for novel RA treatment strategies.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Immunology

Background:

  • Ferroptosis, an iron-dependent cell death, involves iron metabolism, lipid peroxidation, and antioxidant imbalance.
  • Endoplasmic reticulum stress (ERS) regulates cellular homeostasis via unfolded protein responses.
  • Both ferroptosis and ERS are independently linked to rheumatoid arthritis (RA) pathogenesis.

Purpose of the Study:

  • To review the current understanding of ferroptosis and ERS in RA.
  • To explore the potential correlation and interaction between ferroptosis and ERS in RA.
  • To provide a research reference for developing new RA treatments.

Main Methods:

  • Literature review of studies on ferroptosis, ERS, and RA.
  • Analysis of existing research on the interaction pathways of ferroptosis and ERS.
  • Synthesis of information regarding their roles in RA mechanisms.

Main Results:

  • Ferroptosis and ERS share interaction pathways influencing cell survival and death.
  • Evidence suggests independent roles for ferroptosis and ERS in RA.
  • A direct correlation between ferroptosis and ERS in RA has not been previously reported.

Conclusions:

  • The interplay between ferroptosis and ERS may be a significant factor in RA.
  • Further research into this correlation could reveal novel therapeutic targets for RA.
  • Understanding this connection is crucial for advancing RA treatment strategies.
Keywords:
endoplasmic reticulum stressferroptosislipid peroxidationreactive oxygen speciesrheumatoid arthritisunfolded protein response

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