Update in podocyte biology: putting one's best foot forward.
OBJECTIVE
The rapidly developing field of podocyte cell biology is reviewed, focusing on papers published in the last 12 months.


RESULTS
Four areas of particular progress can be discerned. First, podocytes proliferate during early metanephric development, are quiescent after the capillary loop stage, and re-enter the cell cycle only in the disease group termed collapsing glomerulopathy. We have learned that control of the podocyte cell cycle involves both expression of cell-cycle regulating proteins and the process of cytokinesis. Second, the podocyte slit diaphragm is the final component of the filtration barrier. The structure and maintenance of the slit diaphragm has been a major focus of research activity, and a multiplicity of relevant molecular interactions have been defined. Significant advances have been made in understanding the complex and interacting role of nephrin and podocin mutations in the genesis of clinical glomerular disease. Third, several proteins essential to controlling discrete podocyte transcriptional programs have been defined. Finally, conditionally-immortalized podocyte cell lines, derived from mouse and human tissue, have proven their worth as models to advance investigations of podocyte biology.


CONCLUSIONS
Podocyte injury occurs as a consequence of genetic mutation, immunological injury, viral infection, or abnormal hemodynamic forces within the glomerulus. As we understand more about the podocyte proteome and cell biology, we gain an increasingly detailed molecular understanding of podocyte structure and function. In this drama we have many molecular players and increasing stretches of molecular dialogue, but the script remains largely to be deciphered. Nevertheless, we do understand the consequences that arise when the podocyte cannot put its best foot (processes) forward.
Barisoni
Laura
L
The Johns Hopkins University, Baltimore, Maryland, USA.
Kopp
Jeffrey B
JB
D000818:Animals; D001485:Basement Membrane / Q000502:physiology; D002448:Cell Adhesion; D002453:Cell Cycle; D002478:Cells, Cultured; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins; D007674:Kidney Diseases / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000166:cytology* / Q000293:injuries / Q000502:physiology; D008565:Membrane Proteins / Q000235:genetics / Q000502:physiology; D009154:Mutation; D011506:Proteins / Q000235:genetics / Q000502:physiology; D014158:Transcription, Genetic
D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; C407223:NPHS2 protein; D011506:Proteins; C113267:nephrin