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  • Tenascin-C-mediated suppression of extracellular matrix adhesion force promotes entheseal new bone formation through activation of Hippo signalling in ankylosing spondylitis

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Tenascin-C-mediated suppression of extracellular matrix adhesion force promotes entheseal new bone formation through activation of Hippo signalling in ankylosing spondylitis
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  • Published on: 7 September 2021
    Letter to editor: Correspondence on “Tenascin-C-mediated suppression of extracellular matrix adhesion force promotes entheseal new bone formation through activation of Hippo signalling in ankylosing spondylitis” by Li Z, Chen S, Cui H, et al.
    • Kuan-Kai Tung, Orthopedic Surgeon Department of Orthopedics, Taichung Veterans General Hospital, Taichung, Taiwan
    • Other Contributors:
      • Yung-Heng Lee, Orthopedic Surgeon
      • James Cheng-Chung Wei, Immunologist, Deputy Hospital Administrator

    Dear editor:
    We read with great interest the recent article titled ‘‘Tenascin-C-mediated suppression of extracellular matrix adhesion force promotes entheseal new bone formation through activation of Hippo signalling in ankylosing spondylitis’’ by Dr. Li and colleagues1. Authors proposed that excessive Tenascin-C (TNC) deposition at chronic inflammation entheseal site promotes pathological bone formation in ankylosing spondylitis (AS). Suppression of this aberrant pathway may have therapeutic effects in AS. This study provides valuable and innovative results, but some concerns should be taken into account.

    First, the pathophysiological roles of human leukocyte antigen-B27 (HLA-B27)-mediated activation in AS has not been discussed in the study. HLA-B27 was known as a pivotal genetic predisposing factor in AS through the activation of the interleukin (IL)-17/IL-23 axis. By alternating the balance of IL-17- and IL-22-producing cells,2 3 the disruption of the gut microbiome or invasion by pathogenic bacteria might lead to inflammatory or immune-mediated diseases. The misfolding of HLA-B27 mediates the stromal activation in the pathogenesis of syndesmophyte formation of ankylosing spines via upregulating the phosphorylated -inositol-requiring 1 (IRE1)/spliced X-box–binding protein 1 (sXBP1)/retinoic acid receptor-β (RARB)/tissue-nonspecific alkaline phosphatase (TNAP) pathway.4 The enhanced expression of TNAP is a significant factor of abnormal mineralization, and...

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    Conflict of Interest:
    None declared.