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Related Experiment Video

Updated: Jul 14, 2025

Author Spotlight: Evaluating Traditional Chinese Therapy for Ankylosing Spondylitis in Mice
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Association between ankylosing spondylitis and m6A methylation.

Zhiwei Luan1,2, Yansong Wang3,4

  • 1Department of Spine Surgery, The First Affiliated Hospital of Harbin Medical University, Harbin, China.

Journal of Orthopaedic Surgery and Research
|October 7, 2023
PubMed
Summary

Ankylosing spondylitis (AS) is linked to N6-methyl adenosine (m6A) methylation. Key m6A genes negatively correlate with AS incidence, suggesting a role for m6A in AS immunity and treatment.

Keywords:
Ankylosing spondylitisBioinformaticsN6-methyladenosine

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Area of Science:

  • Molecular Biology
  • Immunology
  • Genetics

Background:

  • N6-methyl adenosine (m6A) is the most prevalent reversible mRNA modification in eukaryotes.
  • m6A modification plays crucial roles in diverse biological processes.
  • The association between m6A methylation and ankylosing spondylitis (AS) requires further investigation.

Purpose of the Study:

  • To investigate the relationship between m6A methylation and ankylosing spondylitis (AS).
  • To identify m6A-related genes associated with AS.
  • To explore the potential role of m6A in AS pathogenesis and immunity.

Main Methods:

  • Analysis of 72 samples (52 AS patients, 20 healthy controls) from dataset GSE73754.
  • Screening of 26 m6A-related genes and identification of seven AS-associated signature genes using a random forest model.
  • Immune analysis, gene ontology, and KEGG enrichment analyses were performed.

Main Results:

  • Seven m6A signature genes associated with AS were identified.
  • The nomogram indicated a negative correlation between these AS-related genes and AS incidence.
  • AS showed potential associations with immune system regulation.

Conclusions:

  • The study identified AS-related genes linked to m6A methylation.
  • Findings suggest a negative correlation between specific m6A genes and AS development.
  • The results provide insights into the potential involvement of m6A and immunity in AS, offering avenues for future treatment strategies.