Concept Library

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).

This multi-omics study reveals GALNS depletion as a potential pro-fibrotic molecule following anti-VEGF therapy in proliferative diabetic retinopathy (PDR), offering a promising candidate for perioperative risk stratification.

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

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.

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.

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).

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

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.

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

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

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

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

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

Following intracameral injection of recombinant adeno-associated virus (rAAV) serotypes, virions remain largely contained within the injected eye in wild-type C57BL/6J mice.

Intracameral injection of recombinant adeno-associated virus (rAAV) serotype rAAV2/5 differentially targets the corneal endothelium in wild-type C57BL/6J mice.

Intracameral injection of recombinant adeno-associated virus (rAAV) serotypes rAAV2/7 and rAAV2/8 differentially target the corneal stroma in wild-type C57BL/6J mice.

Intracameral injection of recombinant adeno-associated virus (rAAV) serotypes rAAV2/2 and related capsid mutants differentially target the iris in wild-type C57BL/6J mice.

AFAP1 and FMNL2 were identified as key susceptibility genes for primary open-angle glaucoma (POAG), highlighting FMNL2's regulatory role in aqueous humor outflow pathways, in a comprehensive analysis of 192,702 subjects (15,229 cases and 177,473 controls).

IL-17 signaling appears most prominent during early inflammatory phases across ocular diseases, including glaucoma, while advanced fibrosis may be sustained by IL-17-independent profibrotic circuits.

IL-17 participates in fibrogenic processes through molecular mechanisms including its interaction with transforming growth factor-beta (TGF-beta), facilitation of epithelial-mesenchymal transition, myofibroblast activation, and extracellular matrix deposition.

Interleukin-17 (IL-17) is an immunomodulatory contributor linking chronic inflammation with aberrant tissue remodeling in the eye, including in glaucoma.

Puerarin blocked the activation of the NF-&#x3ba;B pathway by decreasing p-I&#x3ba;B&#x3b1;/p-NF-&#x3ba;B levels in glaucomatous rats.

Puerarin inhibited pro-inflammatory factors (IL-6, TNF-&#x3b1;, IL-1&#x3b2;) and upregulated levels of the anti-inflammatory factor IL-10 in glaucomatous rats.

Puerarin inhibited cell apoptosis in glaucomatous rats by downregulating Bax/Cleaved-Caspase-3 levels and upregulating Bcl-2 levels.

High variability was found between observed biomarkers linked to fibrosis and glaucoma surgery failure due to inconsistencies across studies and differences between aqueous humor, tear fluid, and Tenon.

Overall, failure of glaucoma surgery was more frequently associated with increased levels of pro-inflammatory biomarkers and decreased levels of anti-inflammatory biomarkers.

MCP-1, TGF-β, VEGF, IFN-γ, MMP-3, SPARC, IL-1, IL-2, IL-6, IL-8, IL-10, and IL-18 in aqueous humor, tear fluid, and Tenon showed significant associations with glaucoma surgery outcomes.

Intraocular tumors may hijack the glymphatic system as a bidirectional pathway of communication between the eye and the brain.

Dysfunction of the glymphatic system in the CNS and eye may be a unifying pathogenesis among neurodegeneration, glaucoma, and age-related macular degeneration (AMD).

Hepatocyte growth factor (HGF) confers intrinsic resilience in trabecular meshwork stem cells (TMSCs) and functions as a key, but partial, mediator of their protection of trabecular meshwork (TM) cells.

An HGF receptor inhibitor (HGFI) abolished the protective effect of TMSC-derived secretome (TMSC-Scr) and hepatocyte growth factor (HGF) against oxidative and fibrotic responses to TGF-β2 in TM cells.

TMSC-derived secretome (TMSC-Scr) and hepatocyte growth factor (HGF) markedly reduced oxidative and fibrotic responses to TGF-β2 in TM cells.

RNA sequencing and cytokine analyses identified significant enrichment of HGF in human TMSCs and TMSC-derived secretome (TMSC-Scr).

Compared with TM cells, TMSCs exhibited greater survival, better-preserved mitochondrial function, and lower levels of ROS, lipid peroxidation, and fibrotic marker expression after TGF-β2 treatment.

Functional enrichment and colocalization analyses in individuals of European ancestry identified candidate genes related to retinal cell death, including SDCCAG8, PILRB, FBXO46, NUPR1, and JUND, which were not previously associated with elevated intraocular pressure (IOP).

Knockdown of TXNDC5 significantly reduced TGFβ2-induced ocular hypertension in mice.

Knockdown of TXNDC5 significantly reduced TGFβ2-induced extracellular matrix (ECM) protein accumulation in trabecular meshwork (TM) tissues in mice.

The AR7 was able to reverse TGFβ2-induced trabecular meshwork (TM) extracellular matrix (ECM) accumulation.

TXNDC5 was degraded through the molecular chaperone-mediated autophagy (CMA) pathway.

In human trabecular meshwork (TM) cells, TXNDC5 contributed to the accumulation of extracellular matrix (ECM) by increasing the expression of TGFβ R2.

Confocal microscopic analysis confirmed the homing of transplanted Qtracker-labeled human trabecular meshwork stem cells (TMSCs) to both filtering and non-filtering regions of the trabecular meshwork in a saponin-induced cell loss HOCAS model.

Transplantation of cultured human trabecular meshwork stem cells (TMSCs) into a saponin-induced cell loss HOCAS model resulted in a significant increase in trabecular meshwork (TM) cell proliferation (17.94 ± 4.45%) compared to sham treatment (5.29 ± 4.2%).

Transplantation of cultured human trabecular meshwork stem cells (TMSCs) into a saponin-induced cell loss HOCAS model mitigated the outflow resistance and increased outflow by 38%.