Benjamin R. Thomson

This study identifies VEGFA-producing macrophages around Schlemm's canal as a compensatory mechanism maintaining aqueous humor outflow during aging and vascular stress, suggesting TIE2 activation as a therapeutic target.

This study shows that constitutive Yap activation in distal nephron segments disrupts epithelial identity and nephron patterning by altering cell proliferation, lineage boundaries, and gene expression.

This study shows that loss of PROX1 in adult mouse Schlemm's canal leads to permanent ocular hypertension by converting the canal to a vein-like phenotype.

This paper develops a composite hydrogel (C-gel) that enables localized in situ gelation and sustained nanocarrier release in the anterior chamber of the eye, showing 90% polymer retention and over a month of sustained release in mice.

The paper identifies a PIEZO1-ANGPT2-ITGA9 signaling pathway in Schlemm's canal endothelium that regulates intraocular pressure and glaucoma.

This study shows that inactivating PHD enzymes in endothelial cells after ischemic kidney injury promotes maladaptive repair through glycolysis and MCT4, which can be reversed by MCT4 inhibitors.

The paper identifies non-endothelial EMCN-expressing fibroblasts and pericytes in the choroid of mice and humans, showing they are distinct from endothelial cells and have unique gene expression profiles.