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<p>Osteoarthritis (OA) is a degenerative joint disease marked by cartilage breakdown, chondrocyte apoptosis, and extracellular matrix (ECM) degradation. Non-coding RNAs, particularly circular RNAs (circRNAs), are increasingly recognized as key regulators of OA pathogenesis. This study reveals that circFN1 (hsa_circ_0058152) may act as a competing endogenous RNA, sponging miR-19b-3p and suppressing PTEN expression. This mechanism promotes chondrocyte apoptosis, enhances inflammatory responses, and accelerates ECM degradation, driving OA progression. We investigated the circFN1/miR-19b-3p/PTEN axis using in vitro experiments, including CCK-8 assays, qRT-PCR, Western blotting, ELISA, immunofluorescence, dual-luciferase reporter assays, and bioinformatics analyses to validate regulatory relationships and functional effects. Our study demonstrated that circFN1 suppresses chondrocyte proliferation and exacerbates the inflammatory microenvironment. We further revealed that circFN1 aggravates inflammation-induced chondrocyte injury in OA by repressing the miR-19b-3p/PTEN signaling axis. Collectively, we identified a novel circFN1/miR-19b-3p/PTEN pathway that amplifies IL-1β–induced osteoarthritis progression, highlighting its potential as a therapeutic target for OA intervention. This study identifies the circFN1/miR-19b-3p/PTEN axis as a novel regulator of OA progression. circFN1 may serve as a potential biomarker, and targeting this pathway could provide a basis for future therapeutic strategies.</p>

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CircFN1 modulates IL-1β-induced osteoarthritis through the miR-19b-3p/PTEN signaling axis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月29日

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  • Ye Jiang,
  • Qiwei Wang,
  • Xin Yang,
  • Heng Liu,
  • Hao Wu,
  • Meiyuan Wang,
  • Liping Pan,
  • Yongping Cao,
  • Zhichao Meng

摘要

Osteoarthritis (OA) is a degenerative joint disease marked by cartilage breakdown, chondrocyte apoptosis, and extracellular matrix (ECM) degradation. Non-coding RNAs, particularly circular RNAs (circRNAs), are increasingly recognized as key regulators of OA pathogenesis. This study reveals that circFN1 (hsa_circ_0058152) may act as a competing endogenous RNA, sponging miR-19b-3p and suppressing PTEN expression. This mechanism promotes chondrocyte apoptosis, enhances inflammatory responses, and accelerates ECM degradation, driving OA progression. We investigated the circFN1/miR-19b-3p/PTEN axis using in vitro experiments, including CCK-8 assays, qRT-PCR, Western blotting, ELISA, immunofluorescence, dual-luciferase reporter assays, and bioinformatics analyses to validate regulatory relationships and functional effects. Our study demonstrated that circFN1 suppresses chondrocyte proliferation and exacerbates the inflammatory microenvironment. We further revealed that circFN1 aggravates inflammation-induced chondrocyte injury in OA by repressing the miR-19b-3p/PTEN signaling axis. Collectively, we identified a novel circFN1/miR-19b-3p/PTEN pathway that amplifies IL-1β–induced osteoarthritis progression, highlighting its potential as a therapeutic target for OA intervention. This study identifies the circFN1/miR-19b-3p/PTEN axis as a novel regulator of OA progression. circFN1 may serve as a potential biomarker, and targeting this pathway could provide a basis for future therapeutic strategies.