ArticleScientific reports2026
Evaluation of cytotoxicity, wound healing, and anti-inflammatory effects of netarsudil on human corneal epithelial cells.
Article in Scientific reports, 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.
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Authors and funding
8 authors.
Funding
Abstract
This study evaluated the physicochemical properties of the commercial Rhopressa formulation and investigated the dose–response effects of Rhopressa-equivalent dilutions on cell viability, wound healing, and inflammatory signaling in human corneal epithelial (HCE) cells under static in vitro conditions. Rhopressa exhibited an acidic pH of 5.5 and an osmolarity of 275 mOsm/kg, remaining within a near-physiological tonicity range. Exposure to higher Rhopressa-equivalent dilutions (≥ 1% v/v) induced marked cytotoxicity and ultrastructural degeneration characterized by chromatin condensation and cytoplasmic vacuolization. In contrast, an optimal sublethal response zone was identified at the 0.5% Rhopressa-equivalent dilution, which significantly accelerated corneal epithelial wound closure. In a lipopolysaccharide (LPS)-induced injury model, the 0.5% Rhopressa-equivalent dilution exerted protective anti-inflammatory effects by suppressing intracellular reactive oxygen species (ROS) generation and attenuating NF-κB nuclear translocation. These findings demonstrate biphasic epithelial stress–response patterns to Rhopressa-equivalent exposure and provide mechanistic insight for future hypothesis-driven studies on ocular surface safety and formulation-based dosing optimization.
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Registered trials
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