ArticleInvestigative ophthalmology & visual science2026
Scleral Postn Drives Myopia via Promoting Myofibroblast Transdifferentiation.
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. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: We previously found that scleral hypoxia led to a cascade involving glycolysis-lactate-histone H3 lysine 18 lactylation (H3K18la), which contributes to myopia. Since Cut&Tag identified Postn as a primary H3K18la-enriched extracellular matrix (ECM) gene, which encodes the periostin (Postn) protein, this study aimed to investigate whether Postn drives myopia by modulating scleral ECM remodeling. Methods: H3K18la enrichment at the Postn promoter was validated via CUT&Tag-quantitative PCR. Scleral Postn levels were assessed via reverse-transcription quantitative PCR (RT-qPCR) and immunoblotting during form deprivation myopia (FDM) in mice. Gain- or loss-of-function experiments were conducted to evaluate the role of scleral Postn in normal refractive development or FDM. Mechanisms were explored in FDM mice and human scleral fibroblasts (HSFs) using immunoblotting, co-immunoprecipitation, gene manipulation, and recombinant human POSTN (rhPOSTN) protein treatment. Results: H3K18la enrichment in the Postn promoter region and Postn mRNA and protein levels were increased during myopia. In HSFs, POSTN knockdown inhibited the hypoxia- or lactate-induced rise in fibroblast-to-myofibroblast transdifferentiation (FMT) and rescued type I collagen decline. Scleral Postn overexpression induced myopia in mice, while its knockdown attenuated FDM development. Mechanistically, Postn binds to integrin αvβ3 and αvβ5 receptors to activate the AKT signaling pathway, driving FMT and suppressing type I collagen. Conclusions: Scleral Postn contributes to myopia by promoting FMT in the sclera.
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.