GPX7 reduces chondrocyte inflammation and extracellular matrix degradation triggered by IL‑1β, via a mechanism mediated by ferroptosis

• DOI: 10.3892/mmr.2024.13242
• Publication Date: 2024-05-14T12:26:40Z
• Authors: Boyuan Chen; Weihao Fu; Chunyang Jie; Guoxiu Zhang; Zhen Li; Yihai Liu; Shibo Zhou
• Keywords: Inflammation; Glutathione Peroxidase; Chondrocytes; Interleukin-1beta; Osteoarthritis; Ferroptosis; Humans; Apoptosis; Articles; Lipid Peroxidation; Extracellular Matrix; Cell Line

During osteoarthritis (OA), chondrocytes become highly active, with increased matrix synthesis and inflammatory cytokine‑induced catabolic pathways. Early intervention strategies targeting pathological changes may attenuate or halt disease progression. The present study aimed to reveal the role of glutathione peroxidase (GPX)7 in OA. For this purpose, a research model was established by inducing C28/I2 human interleukin (IL)‑1β, expression level GPX7 determined. To explore its roles, cells were transfected gain overexpression. effects overexpression on intracellular inflammation, extracellular (ECM) degradation, apoptosis ferroptosis then evaluated. In addition, treated inducer, erastin, aforementioned phenotypes assessed. decreased response IL‑1β treatment, suppressed cellular ECM degradation apoptosis. Moreover, reduction lipid peroxidation, ferrous ions transferrin indicated that inhibited ferroptosis. Subsequently, found be promoted upon treatment erastin. These findings suggested regulatory mediated pathway involving On whole, revealed reduces IL‑1β‑induced chondrocyte partially through mechanism results lay theoretical foundation for subsequent OA‑related enable development translational