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KDM2B-PP1 Promotes Remyelination and Functional Recovery After Facial Nerve Injury
Huiyue Xu1, Haoqing Yang1, Yangyang Cao1
1Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Beijing Stomatological Hospital, School of Stomatology, Capital Medical University, Beijing, China.
Journal of Oral Rehabilitation
|April 24, 2026
Summary
A novel peptide, KDM2B-PP1, enhances peripheral nerve repair by promoting Schwann cell remyelination and functional recovery after injury. This epigenetic modulator offers a promising therapeutic strategy for peripheral nerve injuries.
Area of Science:
- Neuroscience
- Regenerative Medicine
- Epigenetics
Background:
- Peripheral nerve injury (PNI) leads to lasting sensory and motor deficits due to poor regeneration and remyelination.
- Schwann cells (SCs) are crucial for nerve repair, but their shift from a repair to a myelinating state is critical for recovery.
Purpose of the Study:
- To investigate if KDM2B-PP1, a peptide targeting the KDM2B-EZH2 interaction, can improve SC redifferentiation, remyelination, and functional recovery post-PNI.
Main Methods:
- In vitro: Rat SCs treated with KDM2B-PP1 to assess myelin gene/protein expression, proliferation, apoptosis, and migration.
- In vivo: Rats with facial nerve transection received local KDM2B-PP1 to evaluate remyelination, nerve structure, and functional recovery.
Main Results:
- KDM2B-PP1 disrupted KDM2B-EZH2 interaction, relieving repression of myelin genes and increasing myelin-associated transcripts/proteins (e.g., Olig1) in SCs.
- In vivo, KDM2B-PP1 enhanced myelin sheath formation, improved nerve architecture, and promoted functional recovery post-injury.
- KDM2B-PP1 did not significantly impact SC proliferation, apoptosis, or migration.
Conclusions:
- KDM2B-PP1 acts as an epigenetic modulator, selectively promoting SC-mediated remyelination and functional recovery after PNI.
- This study offers insights into epigenetic regulation of peripheral nerve regeneration.
- KDM2B-PP1 shows potential as a therapeutic agent for PNI.

