ReviewSpinal cord2026
Notch signaling pathway: a key regulator in spinal cord injury pathogenesis and recovery.
Review in Spinal cord, 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
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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.
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Who cites it
0 citing papers in PubMed.
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Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STUDY
designNarrative Review
objectivesAberrant Notch signaling is increasingly recognized as a key regulator of spinal cord injury (SCI) progression. This narrative review aims to synthesize current evidence regarding the multifaceted roles of Notch signaling in post-SCI inflammation, apoptosis, and neural regeneration.
methodsRecent preclinical studies investigating Notch signaling in SCI were comprehensively reviewed, with particular emphasis on its context-dependent effects on tissue repair and secondary injury, as well as therapeutic approaches targeting the Notch pathway.
resultsCurrent evidence suggests that Notch signaling has a dual role following SCI. Physiological Notch activity supports the maintenance, proliferation, and activation of neural stem and progenitor cells, thereby contributing to endogenous regenerative responses. However, sustained or excessive Notch activation promotes astrocytic reactivity and glial scar formation, creating physical and biochemical barriers to axonal regeneration. Notch signaling also modulates neuroinflammation by regulating microglial and astrocytic responses, producing context-dependent effects that may either limit or aggravate secondary tissue damage. Importantly, preclinical studies indicate that pharmacological inhibition of Notch, particularly through γ-secretase inhibitors, can reduce neuronal loss and glial scarring while enhancing functional recovery.
conclusionsNotch signaling acts as a double-edged regulator of SCI pathophysiology. Its therapeutic potential is substantial, but effective intervention will require precise modulation of pathway activity to preserve regenerative functions while limiting detrimental inflammatory and scarring responses.
Identifiers
42918849What 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.