ArticleJournal of neuroinflammation2023
Iron induces B cell pyroptosis through Tom20-Bax-caspase-gasdermin E signaling to promote inflammation post-spinal cord injury.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 39 citations in OpenAlex.
- The mechanism of vascular injury caused by polystyrene microplastics: Involving ferroptosis and metabolomics.iScience · 2026Article
- Ferroptosis-Pyroptosis Crosstalk in Spinal Cord Injury: Molecular Mechanisms, Emerging Connectors, and Staged Therapeutic Perspectives.Journal of molecular neuroscience : MN · 2026Review
- Targeting Gasdermins for Therapeutic Interventions in Central Nervous System Injury.Neurotoxicity research · 2026Review
- Emerging role of copper in the pathophysiology of spinal cord injury.Neural regeneration research · 2026Article
- Unlocking the Secrets of Regulated Cell Death in Large B-Cell Lymphoma Beyond Apoptosis: Signaling Pathways and Therapeutic Options.International journal of molecular sciences · 2026Review
- Dnmt1 Alleviates S1PR1-Mediated Pyroptosis after Spinal Cord Injury through Regulating Pon3 Expression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Review
- P2Y6R Inhibition Induces Microglial M2 Polarization by Promoting PINK1/Parkin-Dependent Mitophagy After Spinal Cord Injury.Molecular neurobiology · 2025Article
- Ferroptosis and pyroptosis are connected through autophagy: a new perspective of overcoming drug resistance.Molecular cancer · 2025Review
- Advances in neutrophil extracellular traps and ferroptosis in sepsis-induced cardiomyopathy.Frontiers in immunology · 2025Review
- Microglial pyroptosis as a therapeutic target after traumatic spinal cord injury: current progress and future directions.Frontiers in immunology · 2025Review
- Mitochondria as the central regulator of cell death in bronchopulmonary dysplasia.Frontiers in physiology · 2025Review
- Macrophage-derived extracellular vesicles transfer mitochondria to adipocytes and promote adipocyte-myofibroblast transition in epidural fibrosis.NPJ Regenerative medicine · 2024Article
- Unraveling the mechanisms underlying diabetic cataracts: insights from Mendelian randomization analysis.Redox report : communications in free radical research · 2024Article
- Mechanism of Mettl14 regulating AIM2 inflammasome activation and neuronal apoptosis and pyroptosis in spinal cord injury by mediating PPARγ m6A methylation.Journal of physiology and biochemistry · 2024Article
- Salidroside promotes the repair of spinal cord injury by inhibiting astrocyte polarization, promoting neural stem cell proliferation and neuronal differentiation.Cell death discovery · 2024Article
- Caffeic acid phenethyl ester inhibits neuro-inflammation and oxidative stress following spinal cord injury by mitigating mitochondrial dysfunction via the SIRT1/PGC1α/DRP1 signaling pathway.Journal of translational medicine · 2024Article
- Implications of Iron in Ferroptosis, Necroptosis, and Pyroptosis as Potential Players in TBI Morbidity and Mortality.ASN neuro · 2024Review
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
backgroundImmune inflammatory responses play an important role in spinal cord injury (SCI); however, the beneficial and detrimental effects remain controversial. Many studies have described the role of neutrophils, macrophages, and T lymphocytes in immune inflammatory responses after SCI, although little is known about the role of B lymphocytes, and immunosuppression can easily occur after SCI.
methodsA mouse model of SCI was established, and HE staining and Nissl staining were performed to observe the pathological changes. The size and morphology of the spleen were examined, and the effects of SCI on spleen function and B cell levels were detected by flow cytometry and ELISA. To explore the specific mechanism of immunosuppression after SCI, B cells from the spleens of SCI model mice were isolated using magnetic beads and analyzed by 4D label-free quantitative proteomics. The level of inflammatory cytokines and iron ions were measured, and the expression of proteins related to the Tom20 pathway was quantified by western blotting. To clarify the relationship between iron ions and B cell pyroptosis after SCI, we used FeSO
resultsSCI could damage spleen function and lead to a decrease in B cell levels; SCI upregulated the expression of Tom20 protein in the mitochondria of B cells; SCI could regulate the concentration of iron ions and activate the Tom20-Bax-caspase-GSDME pathway to induce B cell pyroptosis. Iron ions aggravated CCCP-induced B cell pyroptosis and human B lymphocytoma pyroptosis by activating the Tom20-Bax-caspase-GSDME pathway. DFO could reduce inflammation and promote repair after SCI by inhibiting Tom20-Bax-caspase-GSDME-induced B cell pyroptosis.
conclusionsIron overload activates the Tom20-Bax-caspase-GSDME pathway after SCI, induces B cell pyroptosis, promotes inflammation, and aggravates the changes caused by SCI. This may represent a novel mechanism through which the immune inflammatory response is induced after SCI and may provide a new key target for the treatment of SCI.
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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.