ArticleeLife2021
Anti-fibrotic activity of a rho-kinase inhibitor restores outflow function and intraocular pressure homeostasis.
Article in eLife, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
44 citing papers in PubMed, 1 synthesis or guideline pooled it, 64 citations in OpenAlex.
- Rho kinase inhibitor for primary open-angle glaucoma and ocular hypertension.The Cochrane database of systematic reviews · 2022Pooled it
- Segmental flow responses in glaucomatous trabecular meshwork cells.Biomaterials advances · 2026Article
- Targeting RhoA/ROCK Signaling to Modulate Extracellular Matrix Remodeling in Corneal Endothelial Dystrophies.Investigative ophthalmology & visual science · 2026Article
- Segmental Outflow and Trabecular Meshwork Stiffness in an Ocular Hypertensive Mouse Model.Investigative ophthalmology & visual science · 2026Article
- Possible Effects of Topical Rho-Kinase Inhibitor on Schlemm's Canal Morphology Parameters.Biomedicines · 2026Article
- Segmental outflow and trabecular meshwork stiffness in an ocular hypertensive mouse model.bioRxiv : the preprint server for biology · 2026Article
- A New Vision for Ocular Disease: Stem Cell Strategies in Regenerative Ophthalmology.Stem cell reviews and reports · 2026Review
- Mechano- and Glucocorticoid-Sensitive TREK-1 Channels Regulate Conventional Outflow and Intraocular Pressure.Investigative ophthalmology & visual science · 2025Article
- Article
- TRPV4 controls circadian and pathological ocular hypertension.The Journal of physiology · 2025Article
- Therapeutic Potential of Rho Kinase Inhibitors in Corneal Disease: A Systematic Review of Preclinical and Clinical Studies.Biomedicines · 2025Review
- A new minimally invasive glaucoma surgery namely trabeculotome tunneling trabeculoplasty for steroid-induced glaucoma: a case report.International journal of ophthalmology · 2025Article
- Multifunctional Mesoporous Titanium Dioxide Nanodrug for Corneal Haze Treatment and Its Mechanism.Biomaterials research · 2025Article
- A Scoping Review of Rho Kinase Inhibitors and their Role in Glaucoma Treatment.Current medicinal chemistry · 2025Article
- Dysregulation of septin cytoskeletal organization in the trabecular meshwork contributes to ocular hypertension.JCI insight · 2024Article
- Trabecular Meshwork Abnormalities in a Model of Congenital Glaucoma Due to LTBP2 Mutation.Investigative ophthalmology & visual science · 2024Article
- A Histomorphometric and Computational Investigation of the Stabilizing Role of Pectinate Ligaments in the Aqueous Outflow Pathway.Journal of biomechanical engineering · 2024Article
- TRPV4 subserves physiological and pathological elevations in intraocular pressure.Research square · 2024Article
- Aging and intraocular pressure homeostasis in mice.Aging cell · 2024Article
- A Histomorphometric and Computational Investigation of the Stabilizing Role of Pectinate Ligaments in the Aqueous Outflow Pathway.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
Abstract
Glucocorticoids are widely used as an ophthalmic medication. A common, sight-threatening adverse event of glucocorticoid usage is ocular hypertension, caused by dysfunction of the conventional outflow pathway. We report that netarsudil, a rho-kinase inhibitor, decreased glucocorticoid-induced ocular hypertension in patients whose intraocular pressures were poorly controlled by standard medications. Mechanistic studies in our established mouse model of glucocorticoid-induced ocular hypertension show that netarsudil both prevented and reduced intraocular pressure elevation. Further, netarsudil attenuated characteristic steroid-induced pathologies as assessed by quantification of outflow function and tissue stiffness, and morphological and immunohistochemical indicators of tissue fibrosis. Thus, rho-kinase inhibitors act directly on conventional outflow cells to prevent or attenuate fibrotic disease processes in glucocorticoid-induced ocular hypertension in an immune-privileged environment. Moreover, these data motivate the need for a randomized prospective clinical study to determine whether netarsudil is indeed superior to first-line anti-glaucoma drugs in lowering steroid-induced ocular hypertension.
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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.