Salt, sodium channels, and SGK1

J Clin Invest. 2007 Mar;117(3):592-5. doi: 10.1172/JCI31538.

Abstract

The hormone aldosterone increases extracellular fluid volume and blood pressure by activating epithelial Na+ channels (ENaCs). Serum- and glucocorticoid-induced kinase 1 (SGK1) is an aldosterone-stimulated signaling molecule that enhances distal nephron Na+ transport, in part by preventing the internalization of ENaCs from the plasma membrane. In this issue of the JCI, Zhang et al. demonstrate that SGK1 enhances transcription of the alpha subunit of ENaC by preventing histone methylation, providing an additional mechanism by which SGK1 increases ENaC-mediated Na+ transport in the distal nephron (see the related article beginning on page 773).

Publication types

  • Comment
  • Research Support, N.I.H., Extramural

MeSH terms

  • Aldosterone / metabolism
  • Animals
  • Epithelial Sodium Channels / genetics*
  • Epithelial Sodium Channels / metabolism
  • Gene Expression Regulation*
  • Histones / metabolism
  • Humans
  • Immediate-Early Proteins / physiology*
  • Methylation
  • Mice
  • Nephrons / metabolism*
  • Protein Transport
  • Protein-Serine-Threonine Kinases / physiology*
  • Receptors, Mineralocorticoid / physiology
  • Sodium Chloride / metabolism*
  • Transcription, Genetic

Substances

  • Epithelial Sodium Channels
  • Histones
  • Immediate-Early Proteins
  • Receptors, Mineralocorticoid
  • Sodium Chloride
  • Aldosterone
  • Protein-Serine-Threonine Kinases
  • serum-glucocorticoid regulated kinase