ArticleTissue & cell2025
3D traction force microscopy in human trabecular meshwork tissues: Effects of ROCK and YAP/TAZ inhibition in normal and glaucomatous tissues.
Article in Tissue & cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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
6 citing papers in PubMed.
- Segmental flow responses in glaucomatous trabecular meshwork cells.Biomaterials advances · 2026Article
- Differential Cytoskeletal Control of Cell-Collagen Mechanics in High- and Low-Flow Glaucomatous Trabecular Meshwork Cells.ACS applied materials & interfaces · 2026Article
- Composition Matters: Collagen vs Polyacrylamide Modulates Distinct Trabecular Meshwork Cell Traction.ACS biomaterials science & engineering · 2026Article
- Segmental Mechanobiology of Normal and Glaucomatous Human Trabecular Meshwork Cells.ACS measurement science au · 2026Article
- Flow-dependent traction in high- and low-flow normal trabecular meshwork cells.Acta biomaterialia · 2026Article
- Actin-microtubule synergy dominates force transmission and collagen strain in human trabecular meshwork.Acta biomaterialia · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Primary open-angle glaucoma (POAG) is the leading cause of irreversible blindness worldwide, with an estimated 112 million people projected to be affected by 2040. The primary risk factor for POAG is elevated intraocular pressure (IOP), which is primarily driven by increased resistance to aqueous humor outflow through the conventional outflow pathway. Despite its prevalence, the precise biomechanical mechanisms underlying this resistance remain unclear. In this study, we utilized 3D in situ traction force microscopy to investigate the effects of the rho kinase (ROCK) inhibitor Y-27632 and the YAP/TAZ inhibitor Verteporfin treatments on the trabecular meshwork (TM) and juxtacanalicular tissue (JCT) cellular contractility and their extracellular matrix (ECM) reorganization in both normal and glaucomatous human donor eyes. Our analysis revealed dysregulated traction forces within glaucomatous tissues, leading to significant ECM reorganization that may contribute to disrupting the homeostasis of the aqueous outflow pathway. Treatments appear to help restore normal ECM structure by adjusting cellular forces. The effect on contractile forces differed between genders, suggesting the significance of gender in treatment response. Our results suggest that targeting these biomechanical pathways may offer new therapeutic strategies to reduce outflow resistance, laying the groundwork for future therapies aimed at preserving vision by restoring ECM biomechanics and improving outflow.
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.