ArticleHeliyon2024
Knockout of TNF-α in microglia decreases ferroptosis and convert microglia phenotype after spinal cord injury.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- M2 polarization of macrophages: Manipulation of spinal cord injury repair.Neural regeneration research · 2026Article
- Advances in ferroptosis and cuproptosis: implications for spinal cord injury.Molecular biology reports · 2026Review
- LncRNA NORAD Promotes Spinal Cord Injury via miR-22-3p/PTEN Axis to Regulate Oxidative Stress and Inflammation in Neuronal Cells.Global spine journal · 2026Article
- PINK1/Parkin-dependent mitophagy mediates astrocytic inflammatory responses to mitochondrial damage.bioRxiv : the preprint server for biology · 2026Article
- Spatiotemporal Co-Delivery of Hydrogen and Magnesium via Microneedle Patches for Neuroinflammation Modulation After Spinal Cord Injury: A Multi-Modal In Vivo Study.Small (Weinheim an der Bergstrasse, Germany) · 2026Article
- Temporal regulation of macrophage polarization by abnormally innervated CGRP + Sensory nerves following spinal cord injury.Cellular and molecular life sciences : CMLS · 2026Review
- Dynamic activation of lytic cell death-related programs identifies CD14 as a candidate hub gene associated with secondary injury after spinal cord injury.Frontiers in immunology · 2026Article
- Ferroptosis in Human Diseases: Fundamental Roles and Emerging Therapeutic Perspectives.Antioxidants (Basel, Switzerland) · 2025Review
- Precision Recovery After Spinal Cord Injury: Integrating CRISPR Technologies, AI-Driven Therapeutics, Single-Cell Omics, and System Neuroregeneration.International journal of molecular sciences · 2025Review
- Enhanced inhibition of neuronal ferroptosis and regulation of microglial polarization with multifunctional traditional Chinese medicine active ingredients-based selenium nanoparticles for treating spinal cord injury.Materials today. Bio · 2025Article
- Amantadine modulates novel macrophage phenotypes to enhance neural repair following spinal cord injury.Journal of translational medicine · 2025Article
- Microglia and programmed cell death in spinal cord injury: beyond apoptosis.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) is a serious and difficult to treat traumatic disease of the central nervous system. Spinal cord injury causes a variety of detrimental effects, including neuroinflammation and ferroptosis, leading to chronic functional impairment and death. Recent studies have shown that microglia/macrophages (M/Ms) at the injury site remain primarily in the pro-inflammatory state, which is detrimental to recovery. However, information on the factors behind pro-inflammatory polarization skew in the injured spinal cord remains unclear. In this study, we found that Tumor Necrosis Factor-α(TNF-α) ablation protected after SCI by suppressing neuroinflammation and ferroptosis. Though using TNF-α knock out mice (TNF-/-), we induced downregulation of TNF-α in M/Ms and further investigated its effect on SCI outcome. In TNF-/- mice, significant behavioral improvements were observed as early as 7 days after injury. We showed that TNF-α inhibition promote injury-mediated M/Ms polarization from pro-inflammatory to anti-inflammatory phenotype in vivo. Furthermore, accumulated iron in M/Ms after SCI increased the expression of TNF-α and the population of M/Ms to pro-inflammatory phenotype. Moreover, zinc supplement reduced the secondary damage caused by iron overload. In conclusion, we found that knock out of TNF-α promotes recovery of motor function after spinal cord injury in mice by inhibiting ferroptosis and promoting the shift of macrophages to an anti-inflammatory phenotype, indicating that there is great potential for this therapy to SCI.
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