ReviewJournal of molecular neuroscience : MN2026
Ferroptosis-Pyroptosis Crosstalk in Spinal Cord Injury: Molecular Mechanisms, Emerging Connectors, and Staged Therapeutic Perspectives.
Review in Journal of molecular neuroscience : MN, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Secondary injury after spinal cord injury (SCI) develops through intertwined oxidative, metabolic and inflammatory processes that engage several programmes of regulated cell death. Ferroptosis and pyroptosis are both implicated in experimental SCI, but their relationship across cellular compartments and injury phases remains incompletely understood. Ferroptotic injury is prominent in neurons, oligodendrocyte-lineage cells and vascular endothelium. Inflammasome-gasdermin signalling is concentrated mainly in microglia and infiltrating myeloid cells. Their partial cellular separation raises the possibility that coupling occurs through shared lesion stress and communication between neighbouring populations. This review examines how metabolic, redox and inflammatory disturbances shape ferroptosis-pyroptosis coupling across cells and over time, and distinguishes common upstream regulation from direct cross-pathway control. The emerging picture is one of context-dependent metabolic-inflammatory coupling, with the strength and direction of interaction likely to vary across lesion compartments and injury phases. Clinical translation will depend on identifying where and when each pathway is active and on developing biomarkers and treatment strategies matched to lesion biology.
Indexed as
Identifiers
42776323What OpenQuestion holds
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.