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Methylation of PRDX3 Expression Alleviate Ferroptosis and Oxidative Stress in Patients with Osteoarthritis Cartilage Injury
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Background/Aims: Osteoarthritis features cartilage degeneration, synovial fibrosis, and bone remodeling. Long-term Western therapies may worsen cartilage damage. We investigated PRDX3’s role in ferroptosis and oxidative stress in osteoarthritis cartilage injury.
Materials and Methods: In osteoarthritis models, PRDX3 expression was downregulated. Single-cell analysis showed PRDX3 in patient bone cells.
Results: Sh-PRDX3 promoted cartilage injury via oxidative stress induction. PRDX3 suppressed ROS accumulation and mitochondria-dependent ferroptosis in vitro and mouse models. PRDX3 induced SIRT3 to reduce SIRT3 ubiquitination. METTL3-mediated m6A modification decreased PRDX3 mRNA stability via YTHDF1.
Conclusion: METTL3-mediated m6A decreases PRDX3 mRNA stability to relieve ferroptosis and oxidative stress in osteoarthritis models. Targeting METTL3 may be therapeutic.
Title: Methylation of PRDX3 Expression Alleviate Ferroptosis and Oxidative Stress in Patients with Osteoarthritis Cartilage Injury
Description:
Background/Aims: Osteoarthritis features cartilage degeneration, synovial fibrosis, and bone remodeling.
Long-term Western therapies may worsen cartilage damage.
We investigated PRDX3’s role in ferroptosis and oxidative stress in osteoarthritis cartilage injury.
Materials and Methods: In osteoarthritis models, PRDX3 expression was downregulated.
Single-cell analysis showed PRDX3 in patient bone cells.
Results: Sh-PRDX3 promoted cartilage injury via oxidative stress induction.
PRDX3 suppressed ROS accumulation and mitochondria-dependent ferroptosis in vitro and mouse models.
PRDX3 induced SIRT3 to reduce SIRT3 ubiquitination.
METTL3-mediated m6A modification decreased PRDX3 mRNA stability via YTHDF1.
Conclusion: METTL3-mediated m6A decreases PRDX3 mRNA stability to relieve ferroptosis and oxidative stress in osteoarthritis models.
Targeting METTL3 may be therapeutic.
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