ArticleExperimental cell research2025
Co-delivery of ripasudil and dexamethasone in trabecular meshwork cells for potential prevention of GC-induced ocular hypertension.
Article in Experimental cell research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Segmental Outflow and Trabecular Meshwork Stiffness in an Ocular Hypertensive Mouse Model.Investigative ophthalmology & visual science · 2026Article
- Segmental outflow and trabecular meshwork stiffness in an ocular hypertensive mouse model.bioRxiv : the preprint server for biology · 2026Article
- Gigantol Preserves Lens Biophysical Homeostasis by Restoring Cytoskeletal Integrity and Membrane Fluidity in a Diabetic Cataract Model.International journal of molecular sciences · 2026Article
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.
Funding
Abstract
The purpose of this in vitro study is to investigate whether the co-delivery of Ripasudil (Rip) can suppress the expression of genes related to glaucoma pathogenesis induced by prolonged dexamethasone (Dex) use, which can lead to ocular hypertension and potentially glaucoma formation. The effects of Rip (10 μM) on Dex (100 nM)-treated human trabecular meshwork (TM) cells were tested through co-delivery and sequential treatments using RNA-seq. Genome-wide analysis was performed using gene ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis with Enrichr and DAVID gene analysis tools. Gene enrichment and pathway analysis revealed that Rip, when co-delivered or sequentially delivered with Dex, influenced genes involved in glaucoma-related pathways such as focal adhesion, extracellular matrix (ECM) organization, and regulation of the actin cytoskeleton. Rip treatment downregulated genes like ACTA2, COL11A1, ECM2, MBP, and ANGPTL7, which are associated with increased outflow resistance and elevated intraocular pressure (IOP). Additionally, Rip upregulated ITGA11, a gene that promotes actin cytoskeleton reorganization and TM cell relaxation by inhibiting the Rho-ROCK pathway. Overall, co-delivery or sequential delivery of Rip can reverse or prevent Dex-induced ocular hypertension and glaucoma formation by modulating the expression of glaucoma-related genes at the transcriptional level.
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.