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<p>Temporomandibular joint osteoarthritis (TMJOA) is a disease that affects the TMJ and is associated with degenerative changes in the articular cartilage. Fibroblast-like synoviocytes (FLSs) have been found to contribute to osteoarthritis. Here, we aim to investigate the role of METTL3-mediated FLS senescence in the TMJOA process. TMJOA model rats were successfully generated, displaying typical structural and inflammatory alterations, and primary FLSs were isolated from monosodium iodoacetate (MIA)-induced TMJOA rats; these FLSs were accompanied by increased senescence, attenuated mitophagy, and upregulated METTL3. FLSs from TMJOA rats also induced cartilage degradation. Mechanistically, METTL3 silencing can increase <i>PINK1</i> expression by increasing its RNA stability through m<sup>6</sup>A modification. In addition, we found that METTL3 silencing could delay cellular senescence and promote mitophagy by upregulating PINK1 in bleomycin (BLM)-induced hFLSs. Senescent FLSs can also accelerate pathological progression and cartilage degradation in Sprague–Dawley (SD) rats. This study revealed that METTL3 silencing could suppress the senescence of FLSs and promote mitophagy by mediating m<sup>6</sup>A modification to upregulate PINK1 during TMJOA progression, which might provide a theoretical basis for TMJOA therapy.</p><p></p>

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METTL3-mediated fibroblast-like synoviocytes senescence promotes temporomandibular joint osteoarthritis progression

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月3日

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  • Kun Tian,
  • Qin Du,
  • Jun Guo,
  • Wen Liao,
  • Xianrui Yang,
  • Shuang Lai,
  • Juan Liao,
  • Yandong Mu,
  • Li Xiao

摘要

Temporomandibular joint osteoarthritis (TMJOA) is a disease that affects the TMJ and is associated with degenerative changes in the articular cartilage. Fibroblast-like synoviocytes (FLSs) have been found to contribute to osteoarthritis. Here, we aim to investigate the role of METTL3-mediated FLS senescence in the TMJOA process. TMJOA model rats were successfully generated, displaying typical structural and inflammatory alterations, and primary FLSs were isolated from monosodium iodoacetate (MIA)-induced TMJOA rats; these FLSs were accompanied by increased senescence, attenuated mitophagy, and upregulated METTL3. FLSs from TMJOA rats also induced cartilage degradation. Mechanistically, METTL3 silencing can increase PINK1 expression by increasing its RNA stability through m6A modification. In addition, we found that METTL3 silencing could delay cellular senescence and promote mitophagy by upregulating PINK1 in bleomycin (BLM)-induced hFLSs. Senescent FLSs can also accelerate pathological progression and cartilage degradation in Sprague–Dawley (SD) rats. This study revealed that METTL3 silencing could suppress the senescence of FLSs and promote mitophagy by mediating m6A modification to upregulate PINK1 during TMJOA progression, which might provide a theoretical basis for TMJOA therapy.