ArticleInvestigative ophthalmology & visual science2026
Sfrp2 in Microglia Inhibited S100a8-Mediated Neuroinflammation and Protected Neural Damage Following Retinal Ischemia-Reperfusion.
Article in Investigative ophthalmology & visual science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The Role of S100A8/A9 in Autoimmune Eye Diseases: From Pathogenesis to Targeted Therapy.Investigative ophthalmology & visual science · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: The purpose of this study was to explore retinal Sfrp2 expression, functional roles, and underlying mechanism in retinal ischemia reperfusion (I/R). Methods: We established an I/R mouse model in vivo and a lipopolysaccharide-stimulated BV2 model in vitro. Immunohistochemistry and Western blotting (WB) assessed Sfrp2 expression in human retinal tissue, and WB further evaluated its expression in I/R model. Immunofluorescence staining was used to define its localization. Sfrp2 expression was ablated by Cre-lox mediated conditional deletion in mouse retinal microglia and by siRNA-mediated knockdown in BV2 cells. Hematoxylin and eosin staining, immunofluorescence, and TUNEL staining were applied for evaluating retinal structure, survival of inner retinal neurons, and cell apoptosis, respectively. Retinal function was evaluated by electroretinography. RNA-sequencing, WB, and immunoprecipitation were used to elucidate the underlying mechanisms. Results: Sfrp2 was highly expressed in the retina subjected to I/R injury. Sfrp2 was shown to localize in microglia in an I/R model. Correspondingly, microglial Sfrp2 deficiency exacerbated the retinal structural damage, inner retinal neuronal degeneration, visual dysfunction, and microglia-mediated inflammation in the I/R model. Mechanistically, Sfrp2 deficiency activated TRAF6-TAK1-NF-κB signaling cascade by promoting the TRAF6-TAK1 complex formation, subsequently increasing the expression of downstream inflammatory mediator S100a8. Importantly, S100a8 inhibitor could partially mitigate the retinal injury induced by microglial Sfrp2 deficiency following I/R. Conclusions: Sfrp2 in microglia inhibits TRAF6-TAK1-NF-κB signaling pathway and downstream inflammatory mediator S100a8 thereby attenuating neuroinflammation and protecting the retina in I/R. Sfrp2 may represent a protective strategy for neuronal degeneration in ischemic retinopathy.
Indexed as
Identifiers
What Socratic 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 Socratic graph.