ArticleScientific reports2024
Photoreceptor regeneration occurs normally in microglia-deficient irf8 mutant zebrafish following acute retinal damage.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- Microglia maintain retinal redox homeostasis following ablation of rod photoreceptors in zebrafish.The Journal of biological chemistry · 2026Article
- Oxidative Stress Signaling and Regenerative Responses in a Larval Zebrafish Model of Retinal Light Damage.Antioxidants (Basel, Switzerland) · 2026Article
- Müller glial and microglial responses coupled to recovery of cone photoreceptors following limited cone ablation in zebrafish retina.Scientific reports · 2026Article
- Article
- Priming neuronal regeneration: early adaptive mechanisms in zebrafish CNS injury.Frontiers in molecular neuroscience · 2026Review
- The Zebrafish as a Model for Ocular Translational Research: From Retinal Repair to Regeneration.Cells · 2025Review
- The neuroimmune interface in retinal regeneration.Progress in retinal and eye research · 2025Review
- Microglia response and function in a chronic model of photoreceptor damage.Frontiers in cell and developmental biology · 2025Article
Corrections and comments
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Authors and funding
6 authors.
Funding
Abstract
Microglia are resident immune cells in the central nervous system, including the retina that surveil the environment for damage and infection. Following retinal damage, microglia undergo morphological changes, migrate to the site of damage, and express and secrete pro-inflammatory signals. In the zebrafish retina, inflammation induces the reprogramming and proliferation of Müller glia and the regeneration of neurons following damage or injury. Immunosuppression or pharmacological ablation of microglia reduce or abolish Müller glia proliferation. We evaluated the retinal architecture and retinal regeneration in adult zebrafish irf8 mutants, which have significantly depleted numbers of microglia. We show that irf8 mutants have normal retinal structure at 3 months post fertilization (mpf) and 6 mpf but fewer cone photoreceptors by 10 mpf. Surprisingly, light-induced photoreceptor ablation induced Müller glia proliferation in irf8 mutants and cone and rod photoreceptor regeneration. Light-damaged retinas from both wild-type and irf8 mutants show upregulated expression of mmp-9, il8, and tnfβ pro-inflammatory cytokines. Our data demonstrate that adult zebrafish irf8 mutants can regenerate normally following acute retinal injury. These findings suggest that microglia may not be essential for retinal regeneration in zebrafish and that other mechanisms can compensate for the reduction in microglia numbers.
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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.