ArticleBiomolecules2024
Ischemic Postconditioning Regulates New Cell Death Mechanisms in Stroke: Disulfidptosis.
Article in Biomolecules, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed.
- 3-Hydroxydehydroleucodin ameliorates neuroinflammation and ischemic brain injury by blocking the TRIM21-PRDX1 interaction.Acta pharmacologica Sinica · 2026Article
- Peroxiredoxins in Stroke: Friends and Foes.Cells · 2026Review
- Emerging regulated cell death (cuproptosis, disulfidptosis, and PANoptosis) in ischemic stroke: research progress and translational prospects.Frontiers in cell and developmental biology · 2026Review
- The role of remote ischemic conditioning in ischemic stroke: neuroprotective mechanisms and future directions.Frontiers in immunology · 2026Review
- Disulfidptosis: a new target for central nervous system disease therapy.Frontiers in neuroscience · 2025Review
- NDUFA11 may be the disulfidptosis-related biomarker of ischemic stroke based on integrated bioinformatics, clinical samples, and experimental analyses.Frontiers in neuroscience · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
objectiveStroke poses a critical health issue without effective neuroprotection. We explore ischemic postconditioning's (IPostC) potential to mitigate stroke-induced brain injury, focusing on its interaction with disulfidptosis, a novel cell death pathway marked by protein disulfide accumulation. We aim to clarify IPostC's protective mechanisms against stroke through gene sequencing and experimental analysis in mice.
methodsThrough our initial investigation, we identified 27 disulfidptosis-related genes (DRGs) and uncovered their interactions. Additionally, differential gene analysis revealed 11 potential candidate genes that are linked to disulfidptosis, stroke, and IPostC. Our comprehensive study employed various analytical approaches, including machine learning, functional enrichment analysis, immune analysis, drug sensitivity analysis, and qPCR experiments, to gain insights into the molecular mechanisms underlying these processes.
resultsOur study identified and expanded the list of disulfidptosis-related genes (DRGs) critical to stroke, revealing key genes and their interactions. Through bioinformatics analyses, including PCA, UMAP, and differential gene expression, we were able to differentiate the effects of stroke from those of postconditioning, identifying
conclusionsThese results suggest that the DRGs are interconnected with various cell death pathways and immune processes, potentially contributing to IPostC regulating cell death mechanisms in stroke.
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Registered trials
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