Evidence map›Paper›PMID 26491696›Full record

ReviewBioMed research international2015

Roles of Akt and SGK1 in the Regulation of Renal Tubular Transport.

Nobuhiko Satoh, Motonobu Nakamura, Masashi Suzuki, Atsushi Suzuki, George Seki, Shoko Horita

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.5field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Novel Mutations inCurrent issues in molecular biology · 2024
    Article
  8. Article
  9. Article
  10. Apoptosis regulation by the tyrosine-protein kinase CSK.Frontiers in cell and developmental biology · 2022
    Review
  11. Interactive Actions of Aldosterone and Insulin on Epithelial NaInternational journal of molecular sciences · 2020
    Article
  12. Review
  13. Insulin: Trigger and Target of Renal Functions.Frontiers in cell and developmental biology · 2020
    Review
  14. Article
  15. Article
  16. Review
  17. NaAnnals of translational medicine · 2016
    Article
  18. Hypertension: the missing WNKs.American journal of physiology. Renal physiology · 2016
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Nobuhiko SatohDepartment of Nephrology, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo, Tokyo 113-8655, Japan.
Motonobu NakamuraDepartment of Nephrology, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo, Tokyo 113-8655, Japan.
Masashi SuzukiDepartment of Nephrology, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo, Tokyo 113-8655, Japan.
Atsushi SuzukiDepartment of Nephrology, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo, Tokyo 113-8655, Japan.
George SekiYaizu City Hospital, 1000 Dobara, Yaizu, Shizuoka 425-8505, Japan.
Shoko HoritaDepartment of Nephrology, The University of Tokyo Hospital, 7-3-1 Hongo, Bunkyo, Tokyo 113-8655, Japan.
University of Tokyo Hospital · JPShizuoka University of Welfare · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A serine/threonine kinase Akt is a key mediator in various signaling pathways including regulation of renal tubular transport. In proximal tubules, Akt mediates insulin signaling via insulin receptor substrate 2 (IRS2) and stimulates sodium-bicarbonate cotransporter (NBCe1), resulting in increased sodium reabsorption. In insulin resistance, the IRS2 in kidney cortex is exceptionally preserved and may mediate the stimulatory effect of insulin on NBCe1 to cause hypertension in diabetes via sodium retention. Likewise, in distal convoluted tubules and cortical collecting ducts, insulin-induced Akt phosphorylation mediates several hormonal signals to enhance sodium-chloride cotransporter (NCC) and epithelial sodium channel (ENaC) activities, resulting in increased sodium reabsorption. Serum- and glucocorticoid-inducible kinase 1 (SGK1) mediates aldosterone signaling. Insulin can stimulate SGK1 to exert various effects on renal transporters. In renal cortical collecting ducts, SGK1 regulates the expression level of ENaC through inhibition of its degradation. In addition, SGK1 and Akt cooperatively regulate potassium secretion by renal outer medullary potassium channel (ROMK). Moreover, sodium-proton exchanger 3 (NHE3) in proximal tubules is possibly activated by SGK1. This review focuses on recent advances in understanding of the roles of Akt and SGK1 in the regulation of renal tubular transport.

Indexed as

Signal TransductionAldosteroneAnimalsBiological TransportHumansImmediate-Early ProteinsInsulin Receptor Substrate ProteinsKidney Tubules, ProximalPhosphorylationPotassium Channels, Inwardly RectifyingProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSerum-Glucocorticoid Regulated KinasesSodium-Bicarbonate SymportersSodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersAldosteroneImmediate-Early ProteinsInsulin Receptor Substrate ProteinsIRS2 protein, humanKCNJ1 protein, humanPotassium Channels, Inwardly RectifyingProtein Serine-Threonine KinasesProto-Oncogene Proteins c-aktSerum-Glucocorticoid Regulated KinasesSLC4A4 protein, humanSLC9A3 protein, humanSodium-Bicarbonate SymportersSodium-Hydrogen Exchanger 3Sodium-Hydrogen Exchangers

Identifiers

PMID26491696
PMCPMC4600925
OpenAlexW1950869949

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.