Losing their footing: Rac1 signaling causes podocyte detachment and FSGS

Kidney Int. 2017 Aug;92(2):283-285. doi: 10.1016/j.kint.2017.03.045.

Abstract

Selective modulation of Rho GTPase activity in podocytes recapitulates characteristic features of human nephrosis. Using a mouse model, Robins et al. found that high levels of Rac1 activation in podocytes caused podocyte detachment and glomerulosclerosis. Podocyte Rac1 activity was enhanced in biopsy specimens from patients with nephrosis, and serum from this patient population activated Rac1 in cultured podocytes. These data provide a causal link between podocyte Rac1 activation and human nephrotic diseases.

Publication types

  • Comment

MeSH terms

  • Glomerulosclerosis, Focal Segmental*
  • Humans
  • Nephrosis*
  • Nephrotic Syndrome*
  • Podocytes*
  • rac1 GTP-Binding Protein

Substances

  • RAC1 protein, human
  • rac1 GTP-Binding Protein