Proteinuria: is it all in the foot?
Despite significant advances in our understanding of the molecular structure and composition of the glomerular filtration barrier, the mechanisms underlying the presence of excess protein in the urine (proteinuria) in acquired human kidney diseases remain elusive. In a study appearing in this issue of the JCI, Sever and associates use a combination of biochemical, genetic, and in vivo approaches in mice to demonstrate a pivotal role of cathepsin L and its substrate the GTPase dynamin, in the induction of proteinuria and associated foot process effacement in glomerular podocytes (see the related article beginning on page 2095).
Ronco
Pierre
P
INSERM UMR S 702, University Pierre et Marie Curie, and Department of Nephrology and Dialysis, Tenon Hospital, Paris, France. pierre.ronco@tnn.aphp.fr
D000199:Actins / Q000235:genetics / Q000378:metabolism; D000818:Animals; D056668:Cathepsin L; D002403:Cathepsins / Q000235:genetics / Q000378:metabolism*; D002478:Cells, Cultured; D003546:Cysteine Endopeptidases / Q000235:genetics / Q000378:metabolism*; D003599:Cytoskeleton / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D034281:Dynamins / Q000235:genetics / Q000378:metabolism*; D007674:Kidney Diseases / Q000201:enzymology* / Q000235:genetics / Q000473:pathology; D051379:Mice; D009154:Mutation; D050199:Podocytes / Q000201:enzymology* / Q000473:pathology; D011507:Proteinuria / Q000235:genetics / Q000378:metabolism* / Q000473:pathology
D000199:Actins; D002403:Cathepsins; D003546:Cysteine Endopeptidases; C534281:CTSL protein, human; D056668:Cathepsin L; C534278:Ctsl protein, mouse; D034281:Dynamins