Published in:
01-02-2012 | Review Article
Serum- and glucocorticoid-inducible kinase 1 in the regulation of renal and extrarenal potassium transport
Authors:
Florian Lang, Volker Vallon
Published in:
Clinical and Experimental Nephrology
|
Issue 1/2012
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Abstract
Serum- and glucocorticoid inducible-kinase 1 (SGK1) is an early gene transcriptionally upregulated by cell stress such as cell shrinkage and hypoxia and several hormones including gluco- and mineralocorticoids. It is activated by insulin and growth factors. SGK1 is a powerful regulator of a wide variety of channels and transporters. The present review describes the role of SGK1 in the regulation of potassium (K+) channels, K+ transporters and K+ homeostasis. SGK1-regulated K+ channels include renal outer medullary K+ channel, Kv1.3, Kv1.5, KCNE1/KCNQ1, KCNQ4 and, via regulation of calcium (Ca2+) entry, Ca2+-sensitive K+ channels. SGK1-sensitive transporters include sodium–potassium-chloride cotransporter 2 and sodium/potassium-adenosine triphosphatase. SGK1-dependent regulation of K+ channels and K+ transport contributes to the stimulation of renal K+ excretion following high K+ intake, to insulin-induced cellular K+ uptake and hypokalemia, to inhibition of insulin release by glucocorticoids, to stimulation of mast cell degranulation and gastric acid secretion, and to cardiac repolarization. Thus, SGK1 has a profound effect on K+ homeostasis and on a multitude of K+-sensitive cellular functions.