ArticleNature2017
Stimulation of functional neuronal regeneration from Müller glia in adult mice.
Article in Nature, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 299 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
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Who cites it
299 citing papers in PubMed, 516 citations in OpenAlex.
- Physiological Postnatal Neurogenesis, Development, and Maturation in the Regenerable Retina.The Journal of comparative neurology · 2026Article
- Therapeutic potential of astrocyte transdifferentiated neurons.Neural regeneration research · 2026Article
- Optimization of AAV tools to target Müller glial cells for retinal gene therapy.Molecular therapy. Advances · 2026Article
- Lipid nanoparticles enable mRNA delivery to diverse cell types of the inner Retina.Molecular therapy. Nucleic acids · 2026Article
- Ascl1 Represses Müller Glial and Promotes Rod Photoreceptor Fate Through Repressing Notch Signaling in Late Retinal Progenitor Cells.Investigative ophthalmology & visual science · 2026Article
- Spinal cord regeneration deploys cell-type specific developmental and non-developmental strategies to restore neuron diversity.Nature communications · 2026Article
- FGF Signaling Potentiates Müller Glia for Mammalian Retinal Regeneration.bioRxiv : the preprint server for biology · 2026Article
- Transient YAP activation uncovers the neurogenic potential of proliferative mammalian Müller glia.PNAS nexus · 2026Article
- Mesenchymal-derived neural progenitors underlie localbioRxiv : the preprint server for biology · 2026Article
- In vivo and ex vivo evaluation of the responses of rat Müller glia after injury.Scientific reports · 2026Article
- Age-Related Neurovascular Dysfunction in the Retina and Potential Pathogenic Mechanisms.Investigative ophthalmology & visual science · 2026Review
- Müller glia-mediated regeneration restores neuronal diversity and retinal circuit organization in the adult zebrafish.bioRxiv : the preprint server for biology · 2026Article
- Müller glial and microglial responses coupled to recovery of cone photoreceptors following limited cone ablation in zebrafish retina.Scientific reports · 2026Article
- Histone methyltransferase Setd8 preserves chromatin accessibility to safeguard retinal progenitor cell identity during development.Stem cell reports · 2026Article
- Electrical stimulation combined with p27Kip1 inactivation drives proliferative neurogenic reprogramming of Mueller glia in the adult mouse retina.bioRxiv : the preprint server for biology · 2026Article
- Article
- Direct neuronal reprogramming for neurological diseases: applications, translational Challenges, and future directions.Frontiers in neuroscience · 2026Review
- Stem Cell-Based Interventions for Retinal Ganglion Cell Protection and Regeneration in Glaucoma: A Review of Current Evidence and Future Directions.Ophthalmic research · 2026Review
- Article
- Crosstalk Between Neuronal and Glial Cells in Diabetic Retinopathy: Mechanisms and Implications for Neurodegeneration.Molecular neurobiology · 2025Review
239 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
9 authors at 3 institutions in 1 country.
Funding
Abstract
Many retinal diseases lead to the loss of retinal neurons and cause visual impairment. The adult mammalian retina has little capacity for regeneration. By contrast, teleost fish functionally regenerate their retina following injury, and Müller glia (MG) are the source of regenerated neurons. The proneural transcription factor Ascl1 is upregulated in MG after retinal damage in zebrafish and is necessary for regeneration. Although Ascl1 is not expressed in mammalian MG after injury, forced expression of Ascl1 in mouse MG induces a neurogenic state in vitro and in vivo after NMDA (N-methyl-d-aspartate) damage in young mice. However, by postnatal day 16, mouse MG lose neurogenic capacity, despite Ascl1 overexpression. Loss of neurogenic capacity in mature MG is accompanied by reduced chromatin accessibility, suggesting that epigenetic factors limit regeneration. Here we show that MG-specific overexpression of Ascl1, together with a histone deacetylase inhibitor, enables adult mice to generate neurons from MG after retinal injury. The MG-derived neurons express markers of inner retinal neurons, synapse with host retinal neurons, and respond to light. Using an assay for transposase-accessible chromatin with high-throughput sequencing (ATAC-seq), we show that the histone deacetylase inhibitor promotes accessibility at key gene loci in the MG, and allows more effective reprogramming. Our results thus provide a new approach for the treatment of blinding retinal diseases.
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What 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.