Synaptopodin deficiency exacerbates kidney disease in a mouse model of Alport syndrome

Abstract

Alport syndrome (AS) is a hereditary disease of the glomerular basement with hematuria and proteinuria. Podocytes eventually exhibit foot process effacement, indicating actin cytoskeletal changes. To investigate how cytoskeletal changes impact podocytes, we generated Alport mice lacking synaptopodin, an actin-binding protein in foot processes. Analysis showed a more rapid disease progression, demonstrating that synaptopodin is protective. This suggests that the actin cytoskeleton is a target for therapy in AS and perhaps other glomerular diseases.