SynthesisMolecular neurobiology2026
Endoplasmic Reticulum Stress in Spinal Cord Injury: Pathological Roles, Molecular Targets, and Emerging Treatments: A Systematic Review.
Synthesis in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Integrative single-cell and bulk transcriptomic analyses identify a microglia-associated NAGLU signature linked to disulfidptosis-associated transcriptional patterns after spinal cord injury.Frontiers in immunology · 2026Article
- Blood-spinal cord barrier disruption after spinal cord injury: a time-dependent mechanistic review.Frontiers in cellular neuroscience · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injuries (SCI) are associated with significant physical and economic burdens on individuals and healthcare systems. Research has shown that several molecular and cellular interactions significantly contribute to SCI progression. The initiation and development of SCI are strongly linked to cellular stress mechanisms, notably those associated with the endoplasmic reticulum (ER), which gives rise to the unfolded protein response (UPR). This systematic review discusses the molecular pathways involved in ER stress, particularly the role of the activating transcription factor 6 (ATF6)-mediated apoptosis pathway and the role of CCAAT/enhancer-binding homologous protein (CHOP) in SCI pathogenesis. Prolonged ER stress exacerbates neuronal degeneration and apoptosis, making it a key factor in SCI. Efforts to inhibit this pathway via genetic or pharmacological interventions have shown potential in addressing cellular dysfunction and preventing SCI-related degeneration. Moreover, pharmacological approaches that mitigate ER stress, for example, by promoting protein folding, are promising for enhancing neuronal survival and reducing damage after SCI. Complementary strategies, such as maintaining metabolic health and engaging in physical activity, could also help fortify the spinal cord against ER stress-related damage. These preventive and therapeutic approaches underscore the importance of targeting ER stress to minimize SCI onset and progression, offering valuable insights for improved care and recovery.
Indexed as
Identifiers
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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.