ArticleNature communications2017
Delaying histone deacetylase response to injury accelerates conversion into repair Schwann cells and nerve regeneration.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
49 citing papers in PubMed, 97 citations in OpenAlex.
- KDM2B-PP1 Promotes Remyelination and Functional Recovery After Facial Nerve Injury.Journal of oral rehabilitation · 2026Article
- Neuro-Instructive Hydrogels - A Key to Sensory Innervation in Oral Tissues: A Comprehensive Review.International journal of nanomedicine · 2026Review
- NAA60 facilitates LRRC8A- and LRRC8D-mediated platinum drug uptake.Communications biology · 2025Article
- Histone Acetylation in Central and Peripheral Nervous System Injuries and Regeneration: Epigenetic Dynamics and Therapeutic Perspectives.International journal of molecular sciences · 2025Review
- Basic Pathological Mechanisms in Peripheral Nerve Diseases.International journal of molecular sciences · 2025Review
- The role and mechanism of Schwann cells in the repair of peripheral nerve injury.Cell and tissue research · 2025Review
- The role and mechanism of Schwann cells in the repair of peripheral nerve injury.Cell and tissue research · 2025Review
- Hypoxia-induced conversion of sensory Schwann cells into repair cells is regulated by HDAC8.Nature communications · 2025Article
- Schwann Cell Development and Myelination.Cold Spring Harbor perspectives in biology · 2024Review
- Valproic acid ameliorates cauda equina injury by suppressing HDAC2-mediated ferroptosis.CNS neuroscience & therapeutics · 2024Article
- Peripheral nerve injury repair by electrical stimulation combined with graphene-based scaffolds.Frontiers in bioengineering and biotechnology · 2024Review
- Sodium butyrate does not protect spinal motor neurons from AMPA-induced excitotoxic degeneration in vivo.Disease models & mechanisms · 2023Article
- Discovery of therapeutic targets for spinal cord injury based on molecular mechanisms of axon regeneration after conditioning lesion.Journal of translational medicine · 2023Article
- Pathophysiology of Work-Related Neuropathies.Biomedicines · 2023Review
- Propionate exerts neuroprotective and neuroregenerative effects in the peripheral nervous system.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- Models and methods to study Schwann cells.Journal of anatomy · 2022Review
- Advancing Our Understanding of the Chronically Denervated Schwann Cell: A Potential Therapeutic Target?Biomolecules · 2022Review
- Exploring the function of factor XIII free B subunit: Interactions with complement factors and a novel approach to identify potential binding partners.Research and practice in thrombosis and haemostasis · 2022Article
- Theophylline Induces Remyelination and Functional Recovery in a Mouse Model of Peripheral Neuropathy.Biomedicines · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The peripheral nervous system (PNS) regenerates after injury. However, regeneration is often compromised in the case of large lesions, and the speed of axon reconnection to their target is critical for successful functional recovery. After injury, mature Schwann cells (SCs) convert into repair cells that foster axonal regrowth, and redifferentiate to rebuild myelin. These processes require the regulation of several transcription factors, but the driving mechanisms remain partially understood. Here we identify an early response to nerve injury controlled by histone deacetylase 2 (HDAC2), which coordinates the action of other chromatin-remodelling enzymes to induce the upregulation of Oct6, a key transcription factor for SC development. Inactivating this mechanism using mouse genetics allows earlier conversion into repair cells and leads to faster axonal regrowth, but impairs remyelination. Consistently, short-term HDAC1/2 inhibitor treatment early after lesion accelerates functional recovery and enhances regeneration, thereby identifying a new therapeutic strategy to improve PNS regeneration after lesion.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.