ArticleNature communications2025
Hypoxia-induced conversion of sensory Schwann cells into repair cells is regulated by HDAC8.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed.
- Macrophage Dab1 Links Early Hypoxia to Adaptive Angiogenesis to Drive Peripheral Nerve Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- cGAS-STING pathway modulation: A new hope for neural regeneration.Neural regeneration research · 2026Article
- Anti-lipid peroxidation attenuates Schwann cell repair phenotype and attenuates PNI-like behavior in oral squamous cell carcinoma.Translational cancer research · 2026Article
- The impactful role of the HDACs in the regulation of gene expression and as targets for disease therapy.Science advances · 2026Review
- Sublytic pyroptosis blocks Schwann cell remyelination through caspase-1-mediated Tyro3 cleavage.Journal of neuroinflammation · 2026Article
- Application of PGCL/AP conductive composite scaffold combined with electrical stimulation in neural tissue engineering.Journal of biological engineering · 2026Article
- TRAF7 in signaling and disease: emerging mechanisms and clinical implications.Molecular medicine (Cambridge, Mass.) · 2025Review
- SYK regulates Schwann cell metabolic reprogramming to promote axonal regeneration in immune-mediated neuropathy.Journal of neuroinflammation · 2025Article
- Peripheral nerve injury-induced remodeling of the tumor-associated macrophages promotes immune evasion in breast cancer.Journal of experimental & clinical cancer research : CR · 2025Article
- Pathologic and Therapeutic Schwann Cells.Cells · 2025Review
- Post-translational modifications orchestrate mTOR-driven cell death in cardiovascular disease.Frontiers in cardiovascular medicine · 2025Review
Corrections and comments
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Authors and funding
14 authors.
Funding
Abstract
After a peripheral nerve injury, Schwann cells (SCs), the myelinating glia of the peripheral nervous system, convert into repair cells that foster axonal regrowth, and then remyelinate or re-ensheath regenerated axons, thereby ensuring functional recovery. The efficiency of this mechanism depends however on the time needed for axons to regrow. Here, we show that ablation of histone deacetylase 8 (HDAC8) in SCs accelerates the regrowth of sensory axons and sensory function recovery. We found that HDAC8 is specifically expressed in sensory SCs and regulates the E3 ubiquitin ligase TRAF7, which destabilizes hypoxia-inducible factor 1-alpha (HIF1α) and counteracts the phosphorylation and upregulation of c-Jun, a major inducer of the repair SC phenotype. Our study indicates that this phenotype switch is regulated by different mechanisms in sensory and motor SCs and is accelerated by HDAC8 downregulation, which promotes sensory axon regeneration and sensory function recovery.
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Registered trials
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