ArticleExperimental & molecular medicine2025
Methyl-CpG-binding domain 2 mitigates osteoarthritis through Steap3 promoter methylation and chondrocyte ferroptosis regulation.
Article in Experimental & molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Iron Homeostasis and Liver Diseases.Journal of cellular and molecular medicine · 2026Review
- Review
- Mechanistic study of antisense long non-coding RNAExploration of targeted anti-tumor therapy · 2026Article
Corrections and comments
- Erratum issued
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Extensive research has underscored the pivotal role of DNA methylation in the development of various diseases, including osteoarthritis (OA). DNA methylation is regulated by methylation writers, readers, and erasers. As a crucial methylation reader, methyl-CpG-binding domain2 (MBD2) has been implicated in modulating the occurrence and progression of multiple inflammatory diseases. This study aims to investigate whether MBD2 contributes to the pathogenesis of OA through its regulation of DNA methylation. Our study confirmed that MBD2 was increased in OA cartilage tissues from humans as well as mice with destabilization of the medial meniscus, despite a reduction in its nuclear import. Specific knockout of Mbd2 in cartilage exacerbated cartilage degradation and accelerated OA progression. Mechanistically, RNA sequencing studies demonstrated that the deletion of MBD2 induced ferroptosis in chondrocytes. Subsequent CUT&Tag and reduced representation bisulfite sequencing analyses revealed that MBD2 binds to the Steap3 promoter region and modulates its methylation state in chondrocytes. STEAP3 catalyzes the reduction of ferric iron (Fe
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