Increased endothelin-1 (ET1) and endothelin receptor A (ETA) signaling have been implicated in the pathogenesis of focal segmental glomerulosclerosis (FSGS). Previous studies have suggested that crosstalk between activated podocytes and glomerular endothelial cells (GECs) could contribute to the pathogenesis of FSGS.
Kidney International published a clinical update in Research Highlights on 09 Feb 2026.
The item focuses on Podocyte-derived endothelin-1 and endothelial cell endothelin A receptors are essential for glomerular injury in mouse models of focal segmental glomerulosclerosis.
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