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Updated: Jun 14, 2026

Du-Moxibustion in a Mouse Model of Ankylosing Spondylitis
04:47

Du-Moxibustion in a Mouse Model of Ankylosing Spondylitis

Published on: October 27, 2023

Comment on "Study on the association between Mettl3-modified Piezo1 in CD4+ T cells and inflammatory response in

Xia Qu1, Chunlian Li1, Dujiang Yang1

  • 1Department of orthopedics, The Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, NO.182, Chunhui Road, Longmatan District, Luzhou, Sichuan Province 646000, PR China.

International Immunopharmacology
|June 12, 2026
PubMed

Insights

The study on METTL3, Piezo1, and ankylosing spondylitis (AS) offers intriguing insights but requires further validation. Tissue-specific studies are needed to confirm the role of this pathway in AS pathogenesis and diagnosis.

Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • Ankylosing spondylitis (AS) pathogenesis involves complex immune responses.
  • The methyltransferase-like 3 (METTL3)-mediated m6A modification of Piezo1 in CD4+ T cells has been proposed in AS.
  • Current understanding relies on peripheral blood T cells, potentially missing tissue-specific mechanisms.

Purpose of the Study:

  • To critically evaluate the proposed role of METTL3-Piezo1 axis in ankylosing spondylitis (AS).
  • To assess the pathogenic and diagnostic implications of METTL3-mediated m6A modification of Piezo1 in CD4+ T cells.
  • To highlight the need for tissue-specific validation and mechanistic studies in AS.

Main Methods:

  • Review and critical analysis of existing data on METTL3, Piezo1, and CD4+ T cells in AS.
  • Comparison of peripheral blood findings with known enthesis and synovial pathobiology in AS.
  • Assessment of the limitations of bulk T-cell analysis and diagnostic performance metrics.

Main Results:

  • The study by Ren et al. suggests METTL3-mediated m6A modification of Piezo1 in CD4+ T cells.
  • Peripheral blood analysis may not fully represent AS pathobiology occurring at tissue sites.
  • The diagnostic utility of peripheral Piezo1 requires cautious interpretation due to potential confounding factors.

Conclusions:

  • The proposed METTL3-Piezo1 axis in AS requires further investigation with tissue-relevant models.
  • Mechanistic studies and functional rescue experiments are essential to confirm direct METTL3 regulation.
  • More rigorous validation is needed before this pathway can be established as pathogenic or a diagnostic biomarker in AS.

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