ReviewNeural regeneration research2014
Role of nuclear factor kappa B in central nervous system regeneration.
Review in Neural regeneration research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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
19 citing papers in PubMed, 37 citations in OpenAlex.
- Neuroprotective Effect of Umbelliferone Against Chemotherapy-Induced Neurotoxicity in Rats via Alteration of NF-κB, PPAR-δ, and Mitochondrial Apoptosis Pathways.Molecular neurobiology · 2026Article
- PSMB9 exacerbates chondrocyte injury in osteoarthritis via activation of the NF-κB pathway.Journal of orthopaedic surgery and research · 2026Article
- Protective effect and molecular mechanisms of magnolol in ischemic stroke.Pharmacological reports : PR · 2025Review
- Modulation of microglia activation by the ascorbic acid transporter SVCT2.Brain, behavior, and immunity · 2024Article
- Review
- Molecular Signature of Neuroinflammation Induced in Cytokine-Stimulated Human Cortical Spheroids.Biomedicines · 2022Article
- The Function of NF-Kappa B During Epilepsy, a Potential Therapeutic Target.Frontiers in neuroscience · 2022Review
- KL-FGF23-VD Axis in Improving Late-Onset Alzheimer's Disease by Modulating IKK/NF-Evidence-based complementary and alternative medicine : eCAM · 2022Article
- Study on the Correlation Between NF-κB and Central Fatigue.Journal of molecular neuroscience : MN · 2021Review
- Two Distinct Faces of Vitamin C: AA vs. DHA.Antioxidants (Basel, Switzerland) · 2021Review
- Role of Nuclear Factor Kappa B (NF-κB) Signalling in Neurodegenerative Diseases: An Mechanistic Approach.Current neuropharmacology · 2020Review
- The Prenylflavonoid ENDF1 Overrules Central Nervous System Growth Inhibitors and Facilitates Regeneration of DRG Neurons.Frontiers in cellular neuroscience · 2019Article
- Anti-inflammatory effects of Metformin improve the neuropathic pain and locomotor activity in spinal cord injured rats: introduction of an alternative therapy.Spinal cord · 2018Article
- IKK2/NF-κB signaling protects neurons after traumatic brain injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- RNA Binding Protein Human Antigen R Is Translocated in Astrocytes following Spinal Cord Injury and Promotes the Inflammatory Response.Journal of neurotrauma · 2017Article
- MicroRNA (miRNA) Signaling in the Human CNS in Sporadic Alzheimer's Disease (AD)-Novel and Unique Pathological Features.International journal of molecular sciences · 2015Article
- Article
- Celastrol Ameliorates EAE Induction by Suppressing Pathogenic T Cell Responses in the Peripheral and Central Nervous Systems.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2015Article
- Pathogenic microRNAs Common to Brain and Retinal Degeneration; Recent Observations in Alzheimer's Disease and Age-Related Macular Degeneration.Frontiers in neurology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activation of nuclear factor kappa B (NF-κB) is a hallmark of various central nervous system (CNS) pathologies. Neuron-specific inhibition of its transcriptional activator subunit RelA, also referred to as p65, promotes neuronal survival under a range of conditions, i.e., for ischemic or excitotoxic insults. In macro- and microglial cells, post-lesional activation of NF-κB triggers a growth-permissive program which contributes to neural tissue inflammation, scar formation, and the expression of axonal growth inhibitors. Intriguingly, inhibition of such inducible NF-κB in the neuro-glial compartment, i.e., by genetic ablation of RelA or overexpression of a transdominant negative mutant of its upstream regulator IκBα, significantly enhances functional recovery and promotes axonal regeneration in the mature CNS. By contrast, depletion of the NF-κB subunit p50, which lacks transcriptional activator function and acts as a transcriptional repressor on its own, causes precocious neuronal loss and exacerbates axonal degeneration in the lesioned brain. Collectively, the data imply that NF-κB orchestrates a multicellular program in which κB-dependent gene expression establishes a growth-repulsive terrain within the post-lesioned brain that limits structural regeneration of neuronal circuits. Considering these subunit-specific functions, interference with the NF-κB pathway might hold clinical potentials to improve functional restoration following traumatic CNS injury.
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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.