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Background <p>Post-traumatic osteoarthritis (PTOA) is a degenerative joint disorder initiated by trauma, with chondrocyte dysfunction and extracellular matrix (ECM) degradation as key pathological features. MicroRNA-652-3p (miR-652-3p) has been linked to osteoarthritis progression, but its role in PTOA remains unclear.</p> Objective <p>This study sought to examine the predictive significance of miR-652-3p in PTOA development and elucidate its mechanistic role via targeting γ-glutamyl carboxylase (GGCX).</p> Methods <p>Circulating miR-652-3p concentrations were measured in 100 PTOA cases and 70 healthy individuals using qRT-PCR. Diagnostic performance was evaluated by ROC analysis. Functional assays and rescue experiments were performed in IL-1β-stimulated C-28/12 chondrocytes. Direct targeting of GGCX by miR-652-3p was demonstrated through luciferase reporter assay.</p> Results <p>Elevated miR-652-3p expression was significantly associated with PTOA (<i>P</i> &lt; 0.001), demonstrating high diagnostic performance (AUC = 0.891). Logistic analysis identified its independent prognostic value for poor PTOA outcomes (OR = 4.789, <i>P</i> = 0.006). MiR-652-3p overexpression suppressed chondrocyte proliferation/migration, promoted apoptosis, and disrupted ECM homeostasis. Experimental validation identified GGCX as a direct downstream target of miR-652-3p, where GGCX silencing abolished the beneficial effects of miR-652-3p suppression.</p> Conclusion <p>Our findings demonstrated that miR-652-3p drives PTOA pathogenesis by suppressing GGCX, highlighting its clinical potential as a combined biomarker and therapeutic candidate.</p>

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MicroRNA-652-3p Drives Chondrocyte Dysfunction in Post-Traumatic Osteoarthritis by Targeting γ-Glutamyl Carboxylase (GGCX)

  • 期刊论文

  • 发表日期：

    2026年6月3日

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  • Qinghai Han,
  • Suyi Wei,
  • Hong Wang,
  • Wei He,
  • Shenlong Ma

摘要

Background

Post-traumatic osteoarthritis (PTOA) is a degenerative joint disorder initiated by trauma, with chondrocyte dysfunction and extracellular matrix (ECM) degradation as key pathological features. MicroRNA-652-3p (miR-652-3p) has been linked to osteoarthritis progression, but its role in PTOA remains unclear.

Objective

This study sought to examine the predictive significance of miR-652-3p in PTOA development and elucidate its mechanistic role via targeting γ-glutamyl carboxylase (GGCX).

Methods

Circulating miR-652-3p concentrations were measured in 100 PTOA cases and 70 healthy individuals using qRT-PCR. Diagnostic performance was evaluated by ROC analysis. Functional assays and rescue experiments were performed in IL-1β-stimulated C-28/12 chondrocytes. Direct targeting of GGCX by miR-652-3p was demonstrated through luciferase reporter assay.

Results

Elevated miR-652-3p expression was significantly associated with PTOA (P < 0.001), demonstrating high diagnostic performance (AUC = 0.891). Logistic analysis identified its independent prognostic value for poor PTOA outcomes (OR = 4.789, P = 0.006). MiR-652-3p overexpression suppressed chondrocyte proliferation/migration, promoted apoptosis, and disrupted ECM homeostasis. Experimental validation identified GGCX as a direct downstream target of miR-652-3p, where GGCX silencing abolished the beneficial effects of miR-652-3p suppression.

Conclusion

Our findings demonstrated that miR-652-3p drives PTOA pathogenesis by suppressing GGCX, highlighting its clinical potential as a combined biomarker and therapeutic candidate.