ArticleAmerican journal of physiology. Renal physiology2016
Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC.
Article in American journal of physiology. Renal physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- Dietary salt impairs circadian physiological metabolic adaptations in salt-sensitive hypertension.Function (Oxford, England) · 2026Article
- High-salt diet promotes atopic dermatitis by partially enhancing intestinal SGK1/ENaC signaling and destroying gutFrontiers in cellular and infection microbiology · 2026Article
- The endocytic adaptor ARH facilitates potassium conservation by regulating ROMK and BK.American journal of physiology. Renal physiology · 2025Article
- SMURF1/2 Are Novel Regulators of WNK1 Stability.Kinases and phosphatases · 2024Article
- Inhibition of mTORC2 promotes natriuresis in Dahl salt-sensitive rats via the decrease of NCC and ENaC activity.American journal of physiology. Renal physiology · 2024Article
- Loss of the alpha subunit distal furin cleavage site blunts ENaC activation following NaThe Journal of physiology · 2024Article
- A New Phase for WNK Kinase Signaling Complexes as Biomolecular Condensates.Physiology (Bethesda, Md.) · 2024Review
- Navigating the multifaceted intricacies of the NaPhysiological reviews · 2024Review
- Klotho is highly expressed in the chief sites of regulated potassium secretion, and it is stimulated by potassium intake.Scientific reports · 2024Article
- Renal tubular SGK1 is required to achieve blood pressure surge and circadian rhythm.American journal of physiology. Renal physiology · 2023Article
- Thirty years of the NaCl cotransporter: from cloning to physiology and structure.American journal of physiology. Renal physiology · 2023Review
- KLHL3-dependent WNK4 degradation affected by potassium through the neddylation and autophagy pathway.BMC nephrology · 2023Article
- Blood pressure effects of sodium transport along the distal nephron.Kidney international · 2022Review
- Endothelial sodium channel activation mediates DOCA-salt-induced endothelial cell and arterial stiffening.Metabolism: clinical and experimental · 2022Article
- Does the early aldosterone-induced SGK1 play a role in early Kaliuresis?Physiological reports · 2022Article
- Coordinate adaptations of skeletal muscle and kidney to maintain extracellular [KAmerican journal of physiology. Cell physiology · 2020Article
- WNK bodies cluster WNK4 and SPAK/OSR1 to promote NCC activation in hypokalemia.American journal of physiology. Renal physiology · 2020Article
- The Molecular Genetics of Gordon Syndrome.Genes · 2019Review
- Intracellular chloride: a regulator of transepithelial transport in the distal nephron.Current opinion in nephrology and hypertension · 2019Review
- The interplay of renal potassium and sodium handling in blood pressure regulation: critical role of the WNK-SPAK-NCC pathway.Journal of human hypertension · 2019Review
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
The stimulation of postprandial K(+) clearance involves aldosterone-independent and -dependent mechanisms. In this context, serum- and glucocorticoid-induced kinase (SGK)1, a ubiquitously expressed kinase, is one of the primary aldosterone-induced proteins in the aldosterone-sensitive distal nephron. Germline inactivation of SGK1 suggests that this kinase is fundamental for K(+) excretion under conditions of K(+) load, but the specific role of renal SGK1 remains elusive. To avoid compensatory mechanisms that may occur during nephrogenesis, we used inducible, nephron-specific Sgk1(Pax8/LC1) mice to assess the role of renal tubular SGK1 in K(+) regulation. Under a standard diet, these animals exhibited normal K(+) handling. When challenged by a high-K(+) diet, they developed severe hyperkalemia accompanied by a defect in K(+) excretion. Molecular analysis revealed reduced neural precursor cell expressed developmentally downregulated protein (NEDD)4-2 phosphorylation and total expression. γ-Epithelial Na(+) channel (ENaC) expression and α/γENaC proteolytic processing were also decreased in mutant mice. Moreover, with no lysine kinase (WNK)1, which displayed in control mice punctuate staining in the distal convoluted tubule and diffuse distribution in the connecting tubule/cortical colleting duct, was diffused in the distal convoluted tubule and less expressed in the connecting tubule/collecting duct of Sgk(Pax8/LC1) mice. Moreover, Ste20-related proline/alanine-rich kinase phosphorylation, and Na(+)-Cl(-) cotransporter phosphorylation/apical localization were reduced in mutant mice. Consistent with the altered WNK1 expression, increased renal outer medullary K(+) channel apical localization was observed. In conclusion, our data suggest that renal tubular SGK1 is important in the regulation of K(+) excretion via the control of NEDD4-2, WNK1, and ENaC.
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