ArticleJournal of advanced research2026
Snapin mediates neuronal PANoptosis after mild traumatic brain injury via H
Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
2 citing papers in PubMed, 1 synthesis or guideline pooled it.
- PANoptosis In Microglia and Neurons Following Traumatic CNS Injury: A Systematic Review of Pathological Features and Therapeutic Implications.CNS neuroscience & therapeutics · 2026Pooled it
- Mitochondrial homeostasis imbalance-triggered PANoptosis in traumatic brain and spinal cord injury: from mechanism to therapeutic strategies.Redox biology · 2026Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionTraumatic brain injury (TBI) induces complex secondary neuronal death, yet no specific therapeutic strategies are available to ameliorate post-traumatic neurological dysfunction. PANoptosis is a coordinated cell death pathway involving apoptosis, pyroptosis, and necroptosis; however, it remains unknown whether PANoptosis contributes to mild TBI (mTBI)-induced neuronal death and what precise mechanisms govern this process.
objectiveThis study aimed to investigate whether Snapin regulates neuronal PANoptosis following mTBI and to elucidate its functional mechanism through the hydrogen sulfide (H
methodsWe utilized a controlled cortical impact (CCI) protocol to create a model of mTBI. Neuronal Snapin was conditionally knocked down via AAV-shSnapin. PANoptosis-related proteins were evaluated using immunofluorescence staining and Western blot. Endogenous H
resultsSnapin was significantly upregulated in cortical and hippocampal neurons after mTBI. Knockdown of Snapin attenuated neurodegeneration, reduced PANoptosis-related proteins, and improved neurofunctional recovery. Mechanistically, Snapin bound to CBS, disrupting H
conclusionSnapin promotes mTBI-induced neuronal PANoptosis by disrupting the H
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