W. D. Stamer

This study examines how aging affects intraocular pressure regulation in mice, finding that outflow facility remains stable despite age-related tissue changes.

This study investigates the role of pectinate ligaments in maintaining the biomechanical stability of the aqueous outflow pathway in mice across different ages.

This study investigates how ECM stiffening affects YAP mechanosignaling in SC cells and shows that disrupting YAP signaling improves outflow facility in glaucoma.

The paper shows that oxidative stress in RPE cells leads to exosome-mediated shedding of desmosomes and hemidesmosomes, indicating early blood-retinal barrier dysfunction.

This study shows that YAP/TAZ signaling is involved in TGFβ2-induced dysfunction of Schlemm's canal cells and that inhibiting YAP/TAZ can reduce this dysfunction.

This study shows that ECM stiffness and TGFβ2 regulate YAP/TAZ activity in HTM cells, contributing to glaucoma progression.

This paper develops FLT4-targeted nanocarriers for glaucoma therapy, showing improved IOP reduction and targeted delivery to Schlemms canal cells.

This paper develops a biomimetic HTM hydrogel model to study glaucoma pathology and test therapeutic interventions.

This study shows that netarsudil, a rho-kinase inhibitor, reverses glucocorticoid-induced ocular hypertension by reducing fibrosis and restoring outflow function.

This study identifies Piezo1 channels as critical for mechanosensitivity in trabecular meshwork cells, showing their role in pressure response, calcium signaling, and outflow regulation.

This study uses single-cell RNA sequencing to create a cell atlas of human ocular outflow tissues, identifying 12 cell types and mapping glaucoma-related gene expression.

The paper compares the sensitivity of four probe technologies to measure biomechanical properties of different cellular regions in two cell types under various perturbations.