vtRNA1-1/p62 regulates macrophages autophagy in ankylosing spondylitis

Minxin Jiang1, Jianping Ni1, Xueying Yu1

  • 1Department of Epidemiology and Biostatistics, School of Public Health, Anhui Medical University, Hefei, Anhui, China; The Inflammation and Immune Mediated Diseases Laboratory of Anhui Province, Anhui Medical University, 81 Meishan Road, Hefei, Anhui 230032, China.

Molecular Immunology
|March 8, 2026
PubMed

Insights

This study reveals that decreased vtRNA1-1 and p62 levels are linked to autophagy dysfunction and inflammation in AS patients. This vtRNA1-1/p62 axis offers potential new diagnostic and therapeutic strategies for AS.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Immunology

Background:

  • Autophagy plays a critical role in cellular homeostasis.
  • Imbalances in autophagy are implicated in various diseases, including AS.
  • The molecular mechanisms regulating autophagy in AS require further elucidation.

Purpose of the Study:

  • To investigate the role of the vtRNA1-1/p62 molecular axis in regulating autophagy in AS.
  • To identify novel diagnostic and therapeutic targets for AS based on this axis.
  • To explore the link between noncoding RNA networks, autophagy, and AS pathogenesis.

Main Methods:

  • Analysis of clinical samples (PBMCs) from AS patients and controls.
  • In vitro cell experiments involving vtRNA1-1 depletion.
  • Computational modeling to assess molecular interactions.
  • Measurement of gene and protein expression levels (vtRNA1-1, p62, ATG3, ATG5, LC3B, TNF-α).

Main Results:

  • AS patients showed decreased vtRNA1-1 and p62 levels, with increased ATG3, ATG5, and TNF-α in PBMCs.
  • vtRNA1-1 levels positively correlated with p62 but inversely with ATG3, ATG5, and TNF-α.
  • vtRNA1-1 depletion in vitro reduced p62 and increased ATG3, ATG5, and LC3B.
  • vtRNA1-1 and p62 demonstrated diagnostic value for AS, individually and in combination.

Conclusions:

  • The vtRNA1-1/p62 axis is a key regulator of autophagy in AS.
  • vtRNA1-1 may modulate macrophage autophagy via p62, contributing to AS pathogenesis.
  • The vtRNA1-1/p62 axis represents a promising target for AS diagnostics and therapeutics.