Overexpression of METTL16 improves GPX4 expression in chondrocytes, suggesting a new treatment for ACH.
Overexpression of METTL16 improved bone growth and alleviated ferroptosis of chondrocytes by increasing m⁶A modification of GPX4 mRNA and thus GPX4 expression in chondrocytes. The METTL16/GPX4 axis may be a promising therapeutic approach for ACH treatment.
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Li et al. (2026) studied this question.
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