ArticleScientific reports2016
Retinal Ganglion Cell Loss is Delayed Following Optic Nerve Crush in NLRP3 Knockout Mice.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 75 citations in OpenAlex.
- Retinal glial cells in glaucoma and age-related retinal diseases: Inflammatory responses, disease transitions, and translational perspectives.Neural regeneration research · 2026Article
- Oxidative Stress in Glaucoma: From Pathogenic Mechanisms to Emerging Antioxidant Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- IL-1β-mediated interaction between Müller cells and microglia through CXCL1/5-CXCR2 aggravates visual dysfunction in experimental glaucoma.Journal of neuroinflammation · 2026Article
- Cytokine Gene Polymorphisms in Primary Glaucoma: Insights into Inflammatory Pathways and Future Directions.Molecular neurobiology · 2026Review
- IL-1-mediated vitreous inflammation as an early indicator of retinal ganglion cell loss following acute optic nerve injury.Journal of neuroinflammation · 2026Article
- Self-amplifying RNA therapy encoding CNTF with disulfiram co-delivery promotes optic nerve repair through microglial pyroptosis inhibition and RGC axonal regeneration.Journal of nanobiotechnology · 2026Article
- Vitreous Inflammation as an Early Indicator of Retinal Ganglion Cell Loss Following Acute Optic Nerve Injury in Mice.bioRxiv : the preprint server for biology · 2025Article
- Evaluating the Evidence for Neuroprotective and Axonal Regenerative Activities of Different Inflammatory Cell Types After Optic Nerve Injury.Molecular neurobiology · 2025Review
- Optic Nerve Crush Does Not Induce Retinal Ganglion Cell Loss in the Contralateral Eye.Investigative ophthalmology & visual science · 2025Article
- Dual role of complement in neuronal repair.Frontiers in immunology · 2025Review
- Consistent Intraocular Pressure Reduction by Solid Drug Nanoparticles in Fixed Combinations for Glaucoma Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Optical coherence tomography assessment of disease activity in cryopyrin-associated periodic syndrome.European journal of neurology · 2024Article
- Retrograde AAV-mediated gene modulation reveals chloride intracellular channel proteins as potent regulators of retinal ganglion cell death.Experimental neurology · 2024Article
- CD38 Deficiency Protects Mouse Retinal Ganglion Cells Through Activating the NAD+/Sirt1 Pathway in Ischemia-Reperfusion and Optic Nerve Crush Models.Investigative ophthalmology & visual science · 2024Article
- Regulated Necrosis in Glaucoma: Focus on Ferroptosis and Pyroptosis.Molecular neurobiology · 2024Review
- Characterization of neural damage and neuroinflammation in Pax6 small-eye mice.Experimental eye research · 2024Article
- Longitudinal Analysis of Retinal Ganglion Cell Damage at Individual Axon Bundle Level in Mice Using Visible-Light Optical Coherence Tomography Fibergraphy.Translational vision science & technology · 2023Article
- Glaucoma and microglia-induced neuroinflammation.Frontiers in ophthalmology · 2023Review
- GSK872 and necrostatin-1 protect retinal ganglion cells against necroptosis through inhibition of RIP1/RIP3/MLKL pathway in glutamate-induced retinal excitotoxic model of glaucoma.Journal of neuroinflammation · 2022Article
- High-Mobility Group Box 1 Inhibitor BoxA Alleviates Neuroinflammation-Induced Retinal Ganglion Cell Damage in Traumatic Optic Neuropathy.International journal of molecular sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The NLRP3 inflammasome, a sensor for a variety of pathogen- and host-derived threats, consists of the adaptor ASC (Apoptosis-associated Speck-like protein containing a Caspase Activation and Recruitment Domain (CARD)), pro-caspase-1, and NLRP3 (NOD-Like Receptor family Pyrin domain containing 3). NLRP3-induced neuroinflammation is implicated in the pathogenesis and progression of eye diseases, but it remains unclear whether activation of NLRP3 inflammasome contributes to retinal ganglion cell (RGC) death. Here we examined NLRP3-induced neuroinflammation and RGC survival following partial optic nerve crush (pONC) injury. We showed that NLRP3 was up-regulated in retinal microglial cells following pONC, propagating from the injury site to the optic nerve head and finally the entire retina within one day. Activation of NLRP3-ASC inflammasome led to the up-regulation of caspase-1 and a proinflammatory cytokine, interleukin-1β (IL-1β). In NLRP3 knockout mice, up-regulation of ASC, caspase-1, and IL-1β were all reduced, and, importantly, RGC and axon loss was substantially delayed following pONC injury. The average survival time of RGCs in NLRP3 knockout mice was about one week longer than for control animals. Taken together, our study demonstrated that ablating the NLRP3 gene significantly reduced neuroinflammation and delayed RGC loss after optic nerve crush injury.
Indexed as
Identifiers
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.