Susan E. Quaggin

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 identifies endothelial PHD3 as a regulator of kidney repair after ischemia, showing its role in suppressing inflammation and fibrosis through HIF-dependent mechanisms.

This study uses scRNA-seq to show that Tcf21 is essential for Foxd1+ stromal progenitor differentiation during kidney development, with loss of Tcf21 causing stromal subpopulation depletion and emergence of Emcn-expressing cells.

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

This paper develops dual-ligand micelles for targeted nanocarrier delivery in acute kidney injury, showing enhanced accumulation in injured kidneys and reduced off-target distribution.

This study identifies Tcf21 as essential for Foxd1+ progenitor cells to differentiate into juxtaglomerular cells during kidney development, showing reduced renin expression and altered renal morphology when Tcf21 is inactivated.

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.

This study creates a mouse model overexpressing VEGF-C in kidney progenitor cells, revealing increased lymphangiogenesis and a cystic kidney phenotype resembling human renal lymphangiectasia.

This study shows that inhibiting prolyl hydroxylases with DMOG impairs angiogenic competence of human vascular endothelial cells through metabolic reprogramming.

The paper investigates the role of FOXC2 in neural crest- and endothelial-derived cells in the trabecular meshwork and Schlemms Canal, showing its importance in development and maintenance of the aqueous humor outflow pathway in glaucoma.