EDNRA and focal segmental glomerulosclerosis: In a model of FSGS, podocyte injury initiated by activating Tgfb signaling specifically in podocytes, we showed an increase in the release of endothelin-1 by podocytes, which acted on increased endothelin receptor type A (Ednra) on adjacent glomerular endothelial cells resulted in endothelial cell mitochondrial oxidative stress and endothelial cell dysfunction (121).