ArticleASN neuro
Heme Oxygenase 1 in Schwann Cells Regulates Peripheral Nerve Degeneration Against Oxidative Stress.
Article in ASN neuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Clemastine Restores Myelination Protein Expression in S16 Schwann Cells by Enhancing AMPK Activation and Reducing HBiomolecules & therapeutics · 2026Article
- Stepwise Regulation of Cellular Oxidative Stress via Conductive-Piezoelectric Integrated Microstructured Conduits for Enhanced Nerve Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Polyphenolic Profile and Antioxidant Capacity of Coffee Silverskin Extracts: Insights from HPLC and GC-MS Analyses and Protective Effect in Schwann-like Cells.Antioxidants (Basel, Switzerland) · 2026Article
- Phase-Specific Evaluation of Sciatic Nerve Regeneration in Preclinical Studies: A Review of Functional Assessment, Emerging Therapies, and Translational Value.International journal of molecular sciences · 2025Review
- Pathologic and Therapeutic Schwann Cells.Cells · 2025Review
- The Multi-targeted Effect of Fascaplysin on the Proliferation and Dedifferentiation of Schwann Cells Inhibits Peripheral Nerve Degeneration by Blocking CDK4/6 and Androgen Receptor.Experimental neurobiology · 2024Article
- Role of Oxygen and Its Radicals in Peripheral Nerve Regeneration: From Hypoxia to Physoxia to Hyperoxia.International journal of molecular sciences · 2024Review
- METTL3-Mediated N6-Methyladenosine Modification of lncRNA D26496 Suppresses the Proliferation and Migration of Schwann Cells after Sciatic Nerve Injury.Molecular neurobiology · 2023Article
- Inhibition of Schwann Cell Pyroptosis Promotes Nerve Regeneration in Peripheral Nerve Injury in Rats.Mediators of inflammation · 2023Article
- Enhanced sciatic nerve regeneration by relieving iron-overloading and organelle stress with the nanofibrous P(MMD-co-LA)/DFO conduits.Materials today. Bio · 2022Article
- Investigation of the Hydrogen Sulfide Signaling Pathway in Schwann Cells during Peripheral Nerve Degeneration: Multi-Omics Approaches.Antioxidants (Basel, Switzerland) · 2022Article
- Effects of targeted muscle reinnervation on spinal cord motor neurons in rats following tibial nerve transection.Neural regeneration research · 2022Article
- Iron Metabolism and Ferroptosis in Peripheral Nerve Injury.Oxidative medicine and cellular longevity · 2022Review
- Article
- Acidic fibroblast growth factor attenuates type 2 diabetes-induced demyelination via suppressing oxidative stress damage.Cell death & disease · 2021Article
- Role of CGRP in Neuroimmune Interaction via NF-κB Signaling Genes in Glial Cells of Trigeminal Ganglia.International journal of molecular sciences · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During Wallerian degeneration, Schwann cells lose their characteristic of myelinating axons and shift into the state of developmental promyelinating cells. This recharacterized Schwann cell guides newly regrowing axons to their destination and remyelinates reinnervated axons. This Schwann cell dynamics during Wallerian degeneration is associated with oxidative events. Heme oxygenases (HOs) are involved in the oxidative degradation of heme into biliverdin/bilirubin, ferrous iron, and carbon monoxide. Overproduction of ferrous iron by HOs increases reactive oxygen species, which have deleterious effects on living cells. Thus, the key molecule for understanding the exact mechanism of Wallerian degeneration in the peripheral nervous system is likely related to oxidative stress-mediated HOs in Schwann cells. In this study, we demonstrate that demyelinating Schwann cells during Wallerian degeneration highly express HO1, not HO2, and remyelinating Schwann cells during nerve regeneration decrease HO1 activation to levels similar to those in normal myelinating Schwann cells. In addition, HO1 activation during Wallerian degeneration regulates several critical phenotypes of recharacterized repair Schwann cells, such as demyelination, transdedifferentiation, and proliferation. Thus, these results suggest that oxidative stress in Schwann cells after peripheral nerve injury may be regulated by HO1 activation during Wallerian degeneration and oxidative-stress-related HO1 activation in Schwann cells may be helpful to study deeply molecular mechanism of Wallerian degeneration.
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