ReviewCells2026
The Role of Interleukin-18 After Spinal Cord Injury: Mechanisms and Therapeutic Potential.
Review in Cells, 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
6 authors.
Funding
Abstract
Spinal cord injury (SCI) triggers a secondary injury cascade characterized by neuroinflammation, reactive gliosis, and neuronal apoptosis. While many pro-inflammatory cytokines contributing to this cascade reach peak upregulation within 24 h, Interleukin-18 (IL-18) exhibits a delayed upregulation profile, typically peaking 7 days post-injury. This review examines the temporal regulation and cell-specific roles contributing to the rise in IL-18 after SCI. Following primary insult, damage-associated molecular patterns prime and activate the NLRP3 inflammasome, which in turn drives latent IL-18 secretion. Cellularly, microglia function as the primary producers of IL-18 via the TLR4/p38-MAPK pathway, while astrocytes serve as the primary responders through IL-18R/p65-NF-κβ signaling. The microglia-astrocyte cross-talk propagates reactive gliosis, drives neuropathic pain, facilitates neuronal loss, and potentially contributes to the formation of the astrocytic border. Targeted therapeutic interventions such as upstream inhibition of NLRP3 inflammasome assembly or direct IL-18 neutralization successfully mitigate neuroinflammation. By either inhibiting NLRP3 inflammasome activation or directly neutralizing IL-18, these treatments shift the microglial toward a protective state, restrict histological damage, and significantly improve functional recovery.
Indexed as
Identifiers
What Socratic 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 Socratic graph.