Targeting the podocyte cytoskeleton: from pathogenesis to therapy in proteinuric kidney disease

Nephrol Dial Transplant. 2016 Oct;31(10):1577-83. doi: 10.1093/ndt/gfw021. Epub 2016 Mar 10.


Glomerular injury often incites a progression to chronic kidney disease, which affects millions of patients worldwide. Despite our current understanding of this disease's pathogenesis, there is still a lack of therapy available to curtail its progression. However, exciting new data strongly suggest the podocyte-an actin-rich, terminally differentiated epithelial cell that lines the outside of the glomerular filtration barrier-as a therapeutic target. The importance of podocytes in the pathogenesis of human nephrotic syndrome is best characterized by identification of genetic mutations, many of which regulate the actin cytoskeleton. The intricate regulation of the podocyte actin cytoskeleton is fundamental in preserving an intact glomerular filtration barrier, and this knowledge has inspired new research targeting actin-regulating proteins in these cells. This review will shed light on recent findings, which have furthered our understanding of the molecular mechanisms regulating podocyte actin dynamics, as well as discoveries that have therapeutic implications in the treatment of proteinuric kidney disease.

Keywords: albuminuria; glomerulosclerosis; nephrotic syndrome; podocytes; proteinuria.

Publication types

  • Review

MeSH terms

  • Animals
  • Cytoskeleton / physiology*
  • Disease Progression
  • Glomerular Filtration Barrier / pathology
  • Humans
  • Kidney Diseases / drug therapy
  • Kidney Diseases / pathology*
  • Kidney Glomerulus / pathology
  • Molecular Targeted Therapy
  • Podocytes / metabolism*
  • Proteinuria / drug therapy
  • Proteinuria / pathology*
  • rho GTP-Binding Proteins / metabolism


  • rho GTP-Binding Proteins