ArticleInvestigative ophthalmology & visual science2026
Targeting RhoA/ROCK Signaling to Modulate Extracellular Matrix Remodeling in Corneal Endothelial Dystrophies.
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
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Fuchs endothelial corneal dystrophy (FECD) involves pathological extracellular matrix (ECM) accumulation within Descemet's membrane, leading to guttae formation, endothelial dysfunction, and vision impairment. As current treatment is primarily surgical, we investigated whether Rho-associated protein kinase (ROCK) inhibition can reduce fibrotic ECM remodeling in FECD and related corneal endothelial diseases. Methods: Endothelial cell-Descemet membrane specimens from FECD, pseudophakous bullous keratopathy (PBK), pseudoexfoliation keratopathy (PEX-K), and normal donor corneas were treated ex vivo with ripasudil or comparator ROCK inhibitors (netarsudil, Y-27632). Complementary in vitro studies used human corneal endothelial cells. ROCK activity, ECM expression, matrix metalloproteinase (MMP) activity, and TGF-β/Smad signaling were analyzed using molecular and imaging techniques. Results: Relative to controls, FECD samples showed constitutive ROCK and TGF-β signaling activation. Ripasudil suppressed ROCK activity and downregulated fibrosis-associated ECM components (including collagens I/III, fibronectin, agrin, TGFBI, clusterin, and tenascin-C), while shifting the MMP-tissue inhibitor of metalloproteinases (TIMP) balance to enhance ECM turnover. These effects were accompanied by reduced ECM deposition and attenuation of TGF-β/Smad signaling, alongside broad transcriptional reprogramming related to fibrosis, inflammation, and cytoskeletal dynamics. Similar ECM-modulating effects were observed in PBK and PEX-K, with ripasudil showing the most pronounced effects among tested inhibitors. Conclusions: ROCK activation contributes to pathological ECM alterations in FECD, and its pharmacologic inhibition with ripasudil suppresses pro-fibrotic ECM production, promotes ECM-remodeling pathways, and supports restoration of ECM homeostasis. These findings suggest ROCK inhibition as a promising non-surgical therapeutic strategy for FECD and related corneal endothelial disorders, warranting further validation in preclinical studies.
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.