ArticleInvestigative ophthalmology & visual science2026
Ly93 Inhibits Sphingomyelin Synthesis and Attenuates Inflammation and Injury in Dry Eye Conjunctival Organoids.
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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: We aimed to investigate the pathogenic role of sphingomyelin (SM) in dry eye disease (DED) and evaluate Ly93, an SM synthase inhibitor, as a potential therapy for DED-associated inflammation. Methods: Tear samples from DED patients and healthy participants were analyzed for SM concentrations using liquid chromatography-tandem mass spectrometry. Correlations between SM levels and clinical parameters were evaluated. The effects of SM on normal conjunctival organoids and the therapeutic efficacy of Ly93 on hyperosmolarity-induced DED conjunctival organoids were investigated. SM levels after treatment with Ly93 were also measured. The inflammatory cytokines (IL-1β, IL-6, and MMP-9), signaling pathways (STAT1, nuclear factor-κB, and PI3K), apoptosis (caspase-3 and caspase-9), ferroptosis (Fe2+, GPX4, TFR, and 4-HNE) were analyzed. Results: Tear SM concentrations were significantly elevated in DED patients and positively correlated with disease severity. Exogenous SM upregulated STAT1, IL-1β, IL-6, and inducible nitric oxide synthase expression in conjunctival organoids. Hyperosmolarity-induced DED conjunctival organoids exhibited elevated MMP-9 and IL-1β, activated signaling pathways (nuclear factor-κB, STAT1, and PI3K), increased apoptosis (caspase-3 and caspase-9), and ferroptosis (elevated Fe2+, TFR, and 4-HNE, and decreased GPX4). Ly93 treatment effectively reduced SM levels and attenuated inflammation, apoptosis, and ferroptosis in the DED organoid model. Conclusions: Our study demonstrates that elevated SM promotes ocular surface inflammation and cellular injury. Inhibition of SM synthase by Ly93 alleviates DED-associated inflammation and injury, suggesting that targeting SM metabolism represents a promising therapeutic strategy.
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.