Research discovers how Mettl3-modified Snhg16 worsens osteoarthritis by promoting chondrocyte ferroptosis, suggesting new treatment targets.
Mettl3-mediated m6A modification of Snhg16 facilitated ferroptosis and ECM degradation to aggravate OA process via regulating Snd1/Gpx4 axis, providing a novel target for OA treatment.
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Li et al. (2026) studied this question.
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