ArticleInvestigative ophthalmology & visual science2011
The high-mobility group box-1 nuclear factor mediates retinal injury after ischemia reperfusion.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 65 citations in OpenAlex.
- Bibliometric analysis of T cells in allergic rhinitis.Heliyon · 2024Review
- Therapeutic Correlation of TLR-4 Mediated NF-κB Inflammatory Pathways in Ischemic Injuries.Current drug targets · 2024Review
- N-acetylserotonin alleviates retinal ischemia-reperfusion injuryInternational journal of ophthalmology · 2024Article
- RAGE plays key role in diabetic retinopathy: a review.Biomedical engineering online · 2023Review
- Molecular mechanisms of NMDA excitotoxicity in the retina.Scientific reports · 2023Article
- [Protective effect of melatonin against oxygen-induced retinopathy: a study based on the HMGB1/NF-κB/NLRP3 axis].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023Article
- Various Forms of Programmed Cell Death Are Concurrently Activated in the Population of Retinal Ganglion Cells after Ischemia and Reperfusion.International journal of molecular sciences · 2023Article
- Microbiome Dysbiosis: A Pathological Mechanism at the Intersection of Obesity and Glaucoma.International journal of molecular sciences · 2023Review
- RAGE and its ligand amyloid beta promote retinal ganglion cell loss following ischemia-reperfusion injury.Frontiers in cellular neuroscience · 2023Article
- High-Mobility Group Box 1 Inhibitor BoxA Alleviates Neuroinflammation-Induced Retinal Ganglion Cell Damage in Traumatic Optic Neuropathy.International journal of molecular sciences · 2022Article
- Damage-Associated Molecular Patterns (DAMPs) in Retinal Disorders.International journal of molecular sciences · 2022Review
- Toll-Like Receptor Signalling Pathways and the Pathogenesis of Retinal Diseases.Frontiers in ophthalmology · 2022Review
- Review
- Glycyrrhizin Protects the Diabetic Retina against Permeability, Neuronal, and Vascular Damage through Anti-Inflammatory Mechanisms.Journal of clinical medicine · 2019Article
- [Marginal protection of retinal cells by bisperoxovanadium : Appropriate therapy in the model of retinal ischemia?]Der Ophthalmologe : Zeitschrift der Deutschen Ophthalmologischen Gesellschaft · 2019Article
- Amelioration of Mouse Retinal Degeneration After Blue LED Exposure by Glycyrrhizic Acid-Mediated Inhibition of Inflammation.Frontiers in cellular neuroscience · 2019Article
- PKA regulates HMGB1 through activation of IGFBP-3 and SIRT1 in human retinal endothelial cells cultured in high glucose.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Article
- P2X7 receptor antagonist protects retinal ganglion cells by inhibiting microglial activation in a rat chronic ocular hypertension model.Molecular medicine reports · 2018Article
- HMBG1 as a Driver of Inflammatory and Immune Processes in the Pathogenesis of Ocular Diseases.Journal of ophthalmology · 2018Review
- Epac1 protects the retina against ischemia/reperfusion-induced neuronal and vascular damage.PloS one · 2018Article
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 1 institution in 1 country.
Funding
Abstract
purposeHigh-mobility group protein B1 (Hmgb1) is released from necrotic cells and induces an inflammatory response. Although Hmgb1 has been implicated in ischemia/reperfusion (IR) injury of the brain, its role in IR injury of the retina remains unclear. Here, the authors provide evidence that Hmgb1 contributes to retinal damage after IR.
methodsRetinal IR injury was induced by unilateral elevation of intraocular pressure and the level of Hmgb1 in vitreous humor was analyzed 24 hours after reperfusion. To test the functional significance of Hmgb1 release, ischemic or normal retinas were treated with the neutralizing anti-Hmgb1 antibody or recombinant Hmgb1 protein respectively. To elucidate in which cell type Hmgb1 exerts its effect, primary retinal ganglion cell (RGC) cultures and glia RGC cocultures were treated with Hmgb1. To clarify the downstream signaling pathways involved in Hmgb1-induced effects in the ischemic retina, receptor for advanced glycation end products (Rage)-deficient mice (RageKO) were used.
resultsHmgb1 is accumulated in the vitreous humor 24 hours after IR. Inhibition of Hmgb1 activity with neutralizing antibody significantly decreased retinal damage after IR, whereas treatment of retinas or retinal cells with Hmgb1 induced a loss of RGCs. The analysis of RageKO versus wild-type mice showed significantly reduced expression of proinflammatory genes 24 hours after reperfusion and significantly increased survival of ganglion cell layer neurons 7 days after IR injury.
conclusionsThese results suggest that an increased level of Hmgb1 and signaling via the Rage contribute to neurotoxicity after retinal IR 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.