ArticleCell cycle (Georgetown, Tex.)2019
Blocking Notch signal pathway suppresses the activation of neurotoxic A1 astrocytes after spinal cord injury.
Article in Cell cycle (Georgetown, Tex.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 3 of them syntheses that pooled it.
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
66 citing papers in PubMed, 3 syntheses or guidelines pooled it, 145 citations in OpenAlex.
- Sirtuin1 in Spinal Cord Injury: Regulatory Mechanisms, Microenvironment Remodeling and Therapeutic Potential.CNS neuroscience & therapeutics · 2025Pooled it
- Roles of neuropathology-associated reactive astrocytes: a systematic review.Acta neuropathologica communications · 2023Pooled it
- The core of maintaining neuropathic pain: Crosstalk between glial cells and neurons (neural cell crosstalk at spinal cord).Brain and behavior · 2023Pooled it
- Notch Signaling in Spinal Cord Injury: Mechanistic Insights and Therapeutic Perspectives.Molecular neurobiology · 2026Review
- GATA6 inhibits the periodontitis progression through regulating the Notch signaling pathway.Odontology · 2026Article
- Neural Stem Cell-Derived Exosomes-Transmitted miR-31-5p Promote Functional Recovery of Spinal Cord Injury by Shifting Astrocytes A1/A2 Polarization.Molecular neurobiology · 2026Article
- Reprogramming the Inflammatory Response to Promote Neural Stem Cell Function After Spinal Cord Injury.Molecular neurobiology · 2026Review
- MAFG Induces the Methylation of CRYAB to Promote the Activation of A1 Astrocyte After Spinal Cord Injury.Immunity, inflammation and disease · 2026Article
- Intrathecal STAT3 inhibitor Bt354 ameliorates chronic constriction injury-induced nociceptive sensitization by modulating neuroinflammation.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- A narrative review of the distribution and role of multipotent fibroblasts in penile tissue: implications for regenerative medicine and erectile dysfunction.Translational andrology and urology · 2025Review
- DLK1-expressing neural progenitor cells promote tissue repair and functional recovery after cervical spinal cord injury.Stem cells translational medicine · 2025Article
- Sodium tanshinone IIA sulfonate promotes proliferation and differentiation of endogenous neural stem cells to repair rat spinal cord injury via the Notch pathway.Journal of translational medicine · 2025Article
- Metabolic Reprogramming of Neural Stem Cells by Chiral Nanofiber for Spinal Cord Injury.ACS nano · 2025Article
- Article
- Research Trends and Evolution of Astrocytes in Depression and Antidepressant Treatment: A Bibliometric Analysis.Current neuropharmacology · 2025Article
- Astrocytic DLL4-NOTCH1 signaling pathway promotes neuroinflammation via the IL-6-STAT3 axis.Journal of neuroinflammation · 2024Article
- Review
- Salidroside promotes the repair of spinal cord injury by inhibiting astrocyte polarization, promoting neural stem cell proliferation and neuronal differentiation.Cell death discovery · 2024Article
- [Therapeutic mechanism of basic fibroblast growth factor on spinal cord injury in rats based on the Notch/signal transducer and activator of transcription 3 signaling pathway].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2024Article
- Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) is a catastrophic disease which has complicated pathogenesis including inflammation, oxidative stress and glial scar formation. Astrocytes are the most abundant cells in central nervous system and fulfill homeostatic functions. Recent studies have described a new reactive phenotype of astrocytes, A1, induced by inflammation, which may have negative effects in SCI. As the Notch signaling pathway has been linked to cell differentiation and inflammation, we aimed to investigate its potential role in the differentiation of astrocytes in SCI. Contusive SCI rat model showed elevated A1 astrocyte numbers at the damage site 28 days after SCI and the expression levels of Notch signaling and its downstream genes were upregulated parallelly. Western blotting, RT-qPCR and immunofluorescence revealed that blocking of Notch pathway using γ-secretase blocker (DAPT) suppressed the differentiation of A1 astrocytes. Flow cytometry, and TUNEL staining indicated that DAPT alleviated neuronal apoptosis and axonal damage caused by A1 astrocytes likely through the Notch-dependent release of pro-inflammatory factors. CO-IP and western blotting revealed an interaction between Notch pathway and signal transducer and activator of transcription 3 (Stat3), which played a vital role in differentiation of A1 astrocytes. We conclude that phenotypic transition of A1 astrocytes and their neurotoxity were controlled by the Notch-Stat3 axis and that Notch pathway in astrocytes may serve as a promising therapeutic target for SCI.
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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.