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Introduction · Introduction

Introduction: An Overview of Glaucoma

Shields' Textbook of Glaucoma, 6th edition

Showing 1–20 of 624 articles

13.
Cross-Sectional Study

Conjunctival Venular Hemodynamic Biomarkers in Glaucoma.

Yang Albert, Cano Jennifer, Xu Benjamin et al.

Transl Vis Sci TechnolSep 2025

This study found reduced conjunctival venular blood flow dynamics (velocity, shear rate, stress) in glaucoma patients, suggesting endothelial dysfunction. This non-invasive measure could be a novel biomarker for glaucoma's vascular damage.

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In multivariable analysis, nasal Schlemm's canal area (SCA) and nasal scleral spur length (SSL) were independent positive predictors of nasal anterior scleral thickness at 0-3mm from the scleral spur (AST0) (both p < 0.001; model R² = 0.356).

MechanismCross-sectionalProspective Cross-sectional Studyn=126 participants (56 POAG, 24 OHT, 46 controls)

PTGDS was identified as the hub gene among 15 circadian rhythm-related differentially expressed genes (CRRDEGs) in human trabecular meshwork (TM) transcriptome data.

MechanismBasic ScienceIntegrated Transcriptome Analysisn=Human TM transcriptome data

PTGDS showed significant overexpression in the trabecular meshwork (TM) of an ocular hypertension (OHT) mouse model.

MechanismBasic ScienceIn Vivo Animal Modeln=OHT mouse model

In vitro tests confirmed that aprepitant partially rescued human trabecular meshwork (TM) cell viability from TGFβ-induced fibrotic stress.

TreatmentBasic ScienceIn Vitro Experimentn=Human TM cells

Aprepitant effectively downregulated the expression of both PTGDS and established fibrosis markers in human trabecular meshwork (TM) cells.

MechanismBasic ScienceIn Vitro Experimentn=Human TM cells

In cultured human corneal endothelial cells exposed to menadione (MN), PEDF effectively enhanced cellular viability, attenuated oxidative stress, and improved mitochondria-related functions.

TreatmentBasic ScienceIn vitro studyn=Cultured human corneal endothelial cells

In the UVA-induced FECD mouse model, PEDF pretreatment prevented the decline of corneal endothelial cells and promoted the recovery of endothelial cell density, morphology, and functions.

TreatmentBasic ScienceAnimal model studyn=UVA-induced FECD mouse model

The protective effects of PEDF were associated with the suppression of p53, TGF-β, and Hippo signaling pathways elevated in FECD.

MechanismBasic ScienceBasic science studyn=PEDF-treated HCECs

The aqueous humor of eyes with congenital cataracts with posterior polar abnormality (PPA group, n = 78) showed significantly higher vascular endothelial growth factor A (VEGF-A), fibroblast growth factor 2 (FGF2), and neurotrophin-4 (NT-4) and lower fibroblast growth factor 1 (FGF1) and platelet-derived growth factor-AA (PDGF-AA) compared to non-PPA controls (n = 18) (all q < 0.05, false discovery rate adjusted).

MechanismCohortProspective Cohort Studyn=96 eyes (78 PPA, 18 non-PPA)

Independent validation using PRM proteomics and SRM metabolomics in an independent cohort (10 cataract controls, 5 simple VH, 5 VH + TRD) confirmed that only GALNS was robustly validated across both cross-sectional (P = 0.016) and longitudinal (P = 0.049) comparisons following anti-VEGF therapy in PDR, whereas CAST and 3-HPA did not reach statistical significance.

MechanismCohortValidation Cohort Studyn=20 patients (10 cataract controls, 5 simple VH, 5 VH + TRD)

GALNS exhibited a biphasic pattern, being elevated in proliferative diabetic retinopathy (PDR) relative to cataract controls, yet depleted in vitreous hemorrhage with tractional retinal detachment (VH + TRD), and further declined post-treatment with anti-VEGF therapy.

MechanismCohortLongitudinal Cohort Studyn=25 patients

GALNS knockdown in fibroblasts upregulated α-SMA and collagen I, accelerated migration, and enhanced contractility, indicating GALNS depletion as a potential pro-fibrotic mediator.

MechanismBasic ScienceIn Vitro Studyn=Not applicable (in vitro)