ArticleMolecular neurobiology2026
Every-Other-Day Fasting Prehabilitation Attenuates Secondary Injury Following Spinal Cord Injury and Is Associated with Stage-Dependent SREBP1-Related Metabolic-Immune Remodeling.
Article in Molecular neurobiology, 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) induces secondary damage characterized by metabolic disturbance, excessive inflammation, and progressive neurological dysfunction. Every-other-day fasting (EODF) has shown neuroprotective potential, but the mechanisms underlying its effects in SCI remain unclear. We investigated whether EODF prehabilitation attenuates SCI-associated secondary injury through SREBF1-associated metabolic-immune remodeling. Female C57BL/6 J mice underwent EODF for 4 weeks before SCI induction, and adeno-associated virus-mediated SREBF1 knockdown was used to assess the functional contribution of SREBF1. EODF was well tolerated, significantly improved locomotor recovery, reduced lesion cavity formation, and attenuated histopathological damage after SCI. EODF also had stage-dependent effects on SREBF1 expression, suppressing its aberrant early protein elevation while promoting coordinated regulation at later stages. In parallel, EODF partially restored altered omega-3 and omega-6 fatty acid profiles, attenuated TLR4/MyD88 signaling, reduced TNF-α, increased IL-10, shifted macrophage/microglia-associated markers toward a less proinflammatory profile, and reduced the proportion of TUNEL-positive cells. These protective effects were markedly attenuated by SREBF1 knockdown. Overall, our findings indicate that EODF prehabilitation mitigates SCI-associated secondary injury and support SREBF1-associated metabolic-immune remodeling as a functionally relevant mechanism underlying this protection. The results further suggest that temporal regulation of metabolic-inflammatory coupling may contribute to spinal cord resilience after injury.
Indexed as
Identifiers
What 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.