ArticleFrontiers in ophthalmology2022
Effects of Netarsudil-Family Rho Kinase Inhibitors on Human Trabecular Meshwork Cell Contractility and Actin Remodeling Using a Bioengineered ECM Hydrogel.
Article in Frontiers in ophthalmology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Bioengineered 3D Human Trabecular Meshwork Models for Outflow Physiology and Glaucoma Research.Bioengineering (Basel, Switzerland) · 2026Review
- Human umbilical cord mesenchymal stem cell-derived exosomes prevent and alleviate experimental pulmonary fibrosis by modulating the cytoskeleton of macrophages.Stem cell research & therapy · 2025Article
- TRPV4 activation by TGFβ2 enhances cellular contractility and drives ocular hypertension.eLife · 2025Article
- Divergence in cellular markers observed in single-cell transcriptomics datasets between cultured primary trabecular meshwork cells and tissues.Scientific data · 2025Article
- A Scoping Review of Rho Kinase Inhibitors and their Role in Glaucoma Treatment.Current medicinal chemistry · 2025Article
- Artificial Trabecular Meshwork Structure Combining Melt Electrowriting and Solution Electrospinning.Polymers · 2024Article
- To be or not to be - Decoding the Trabecular Meshwork Cell Identity.bioRxiv : the preprint server for biology · 2024Article
- Targeting YAP/TAZ mechanosignaling to ameliorate stiffness-induced Schlemm's canal cell pathobiology.American journal of physiology. Cell physiology · 2024Article
- Nanofibrous PCL-Based Human Trabecular Meshwork for Aqueous Humor Outflow Studies.ACS biomaterials science & engineering · 2023Article
- Targeting YAP mechanosignaling to ameliorate stiffness-induced Schlemm's canal cell pathobiology.bioRxiv : the preprint server for biology · 2023Article
- Simvastatin Attenuates Glucocorticoid-Induced Human Trabecular Meshwork Cell Dysfunction via YAP/TAZ Inactivation.Current eye research · 2023Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interactions between trabecular meshwork (TM) cells and their extracellular matrix (ECM) are critical for normal outflow function in the healthy eye. Multifactorial dysregulation of the TM is the principal cause of elevated intraocular pressure that is strongly associated with glaucomatous vision loss. Key characteristics of the diseased TM are pathologic contraction and actin stress fiber assembly, contributing to overall tissue stiffening. Among first-line glaucoma medications, the Rho-associated kinase inhibitor (ROCKi) netarsudil is known to directly target the stiffened TM to improve outflow function
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