ArticleNeurobiology of disease2017
Combined chondroitinase and KLF7 expression reduce net retraction of sensory and CST axons from sites of spinal injury.
Article in Neurobiology of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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
17 citing papers in PubMed, 35 citations in OpenAlex.
- Neurons Are Not All the Same: Diversity in Neuronal Populations and Their Intrinsic Responses to Spinal Cord Injury.ASN neuro · 2025Review
- Co-targeting B-RAF and PTEN Enables Sensory Axons to Regenerate Across and Beyond the Spinal Cord Injury.Frontiers in molecular neuroscience · 2022Article
- Modulation of Both Intrinsic and Extrinsic Factors Additively Promotes Rewiring of Corticospinal Circuits after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Locomotor Behavior Analysis in Spinal Cord InjuredVeterinary sciences · 2021Article
- Co-occupancy identifies transcription factor co-operation for axon growth.Nature communications · 2021Article
- Transneuronal delivery of hyper-interleukin-6 enables functional recovery after severe spinal cord injury in mice.Nature communications · 2021Article
- Epac2 Elevation Reverses Inhibition by Chondroitin Sulfate ProteoglycansThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Knockdown of Fidgetin Improves Regeneration of Injured Axons by a Microtubule-Based Mechanism.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- On the development of optical peripheral nerve interfaces.Neural regeneration research · 2019Review
- The Role of Axon Transport in Neuroprotection and Regeneration.Developmental neurobiology · 2018Review
- KLF6 and STAT3 co-occupy regulatory DNA and functionally synergize to promote axon growth in CNS neurons.Scientific reports · 2018Article
- Inhibition of KLF7-Targeting MicroRNA 146b Promotes Sciatic Nerve Regeneration.Neuroscience bulletin · 2018Article
- The altered expression of perineuronal net elements during neural differentiation.Cellular & molecular biology letters · 2018Article
- Targeting Enolase in Reducing Secondary Damage in Acute Spinal Cord Injury in Rats.Neurochemical research · 2017Article
- AAV-KLF7 Promotes Descending Propriospinal Neuron Axonal Plasticity after Spinal Cord Injury.Neural plasticity · 2017Article
- Combinatory transplantation of mesenchymal stem cells with flavonoid small molecule in acellular nerve graft promotes sciatic nerve regeneration.Journal of tissue engineeringArticle
- Comprehensive therapeutics targeting the corticospinal tract following spinal cord injury.Journal of Zhejiang University. Science. BReview
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Axon regeneration in the central nervous system is limited both by inhibitory extracellular cues and by an intrinsically low capacity for axon growth in some CNS populations. Chondroitin sulfate proteoglycans (CSPGs) are well-studied inhibitors of axon growth in the CNS, and degradation of CSPGs by chondroitinase has been shown to improve the extension of injured axons. Alternatively, axon growth can be improved by targeting the neuron-intrinsic growth capacity through forced expression of regeneration-associated transcription factors. For example, a transcriptionally active chimera of Krüppel-like Factor 7 (KLF7) and a VP16 domain improves axon growth when expressed in corticospinal tract neurons. Here we tested the hypothesis that combined expression of chondroitinase and VP16-KLF7 would lead to further improvements in axon growth after spinal injury. Chondroitinase was expressed by viral transduction of cells in the spinal cord, while VP16-KLF7 was virally expressed in sensory neurons of the dorsal root ganglia or corticospinal tract (CST) neurons. After transection of the dorsal columns, both chondroitinase and VP16-KLF7 increased the proximity of severed sensory axons to the injury site. Similarly, after complete crush injuries, VP16-KLF7 expression increased the approach of CST axons to the injury site. In neither paradigm however, did single or combined treatment with chondroitinase or VP16-KLF7 enable regenerative growth distal to the injury. These results substantiate a role for CSPG inhibition and low KLF7 activity in determining the net retraction of axons from sites of spinal injury, while suggesting that additional factors act to limit a full regenerative response.
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Registered trials
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