Proteinuria: is it all in the foot?

Abstract

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).

• Authors: Pierre Ronco
• Journal: The Journal of clinical investigation (J Clin Invest) Vol. 117 Issue 8 Pg. 2079-82 (Aug 2007) ISSN: 0021-9738 [Print] United States
• PMID: 17671644 (Publication Type: Journal Article, Comment)

Chemical References

• Actins
• Cathepsins
• Cysteine Endopeptidases
• CTSL protein, human
• Cathepsin L
• Ctsl protein, mouse
• Dynamins

Topics

• Actins (genetics, metabolism)
• Animals
• Cathepsin L
• Cathepsins (genetics, metabolism)
• Cells, Cultured
• Cysteine Endopeptidases (genetics, metabolism)
• Cytoskeleton (genetics, metabolism, pathology)
• Dynamins (genetics, metabolism)
• Kidney Diseases (enzymology, genetics, pathology)
• Mice
• Mutation
• Podocytes (enzymology, pathology)
• Proteinuria (genetics, metabolism, pathology)