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Related Experiment Video

Updated: Jan 13, 2026

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Interleukin-1β-induced arthritis involves chondrocyte oxiapoptophagy.

Jeong-Yeon Seo1, Do Kyung Kim1, HyangI Lim1

  • 1Department of Oral Physiology, School of Dentistry, Chosun University, Gwangju 61452, Korea.

The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology
|January 7, 2026
PubMed
Summary

Interleukin-1β (IL-1β) triggers a unique cell death called oxiapoptophagy in chondrocytes, leading to articular cartilage degeneration. This process involves oxidative stress, apoptosis, and autophagy, mediated by the NF-κB pathway, and is implicated in arthritis.

Keywords:
ApoptosisAutophagyChondrocyteInterleukin-1betaOxiapoptophagyOxidative stress

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Immunology

Background:

  • Chondrocyte death contributes to arthritis pathogenesis.
  • Oxysterols can induce oxiapoptophagy, a cell death pathway involving oxidative stress, apoptosis, and autophagy.
  • Interleukin-1β (IL-1β) is a key pro-inflammatory cytokine implicated in joint inflammation and cartilage degradation.

Purpose of the Study:

  • To investigate whether IL-1β-induced articular cartilage degeneration involves chondrocyte oxiapoptophagy.
  • To elucidate the molecular mechanisms underlying IL-1β-induced chondrocyte dysfunction and cartilage damage.

Main Methods:

  • Intra-articular injection of IL-1β into experimental animal knee joints.
  • Analysis of cartilage explants and chondrocytes for molecular markers of degeneration, oxysterol metabolism, apoptosis, oxidative stress, and autophagy.
  • Investigation of signaling pathways, including NF-κB, Akt, and mTOR.
  • Pharmacological inhibition of the NF-κB pathway using CDDO-Me.

Main Results:

  • IL-1β induced progressive articular cartilage degeneration and proteoglycan loss.
  • IL-1β upregulated cholesterol-25-hydroxylase (CH25H) and CYP7B1, increasing 25-hydroxycholesterol (25-HC) production.
  • IL-1β promoted chondrocyte apoptosis, oxidative stress (ROS), and autophagy via p53 and altered Akt/mTOR signaling.
  • IL-1β activated the NF-κB pathway, which was critical for the observed molecular changes and chondrocyte damage.
  • NF-κB inhibition suppressed IL-1β-induced markers of oxiapoptophagy and ROS production.

Conclusions:

  • IL-1β-induced articular cartilage degeneration is mechanistically linked to chondrocyte oxiapoptophagy.
  • The NF-κB signaling pathway plays a crucial role in mediating IL-1β-induced chondrocyte oxiapoptophagy and cartilage damage.
  • Targeting the NF-κB pathway may offer a therapeutic strategy for IL-1β-driven arthritic conditions.