Evidence map›Paper›PMID 28679951›Full record

ArticleJCI insight2017

A salt-sensing kinase in T lymphocytes, SGK1, drives hypertension and hypertensive end-organ damage.

Allison E Norlander, Mohamed A Saleh, Arvind K Pandey, Hana A Itani, Jing Wu, Liang Xiao, Jooeun Kang, Bethany L Dale, Slavina B Goleva, Fanny Laroumanie and 3 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

80 citing papers in PubMed, 117 citations in OpenAlex.

  1. Trial
  2. Salt and chronic kidney disease.Nature reviews. Nephrology · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Recent advances on immunity and hypertension: the new cells on the kidney block.American journal of physiology. Renal physiology · 2025
    Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Immunological insights into hypertension: unraveling triggers and potential therapeutic avenues.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Review
  17. Article
  18. Immune and inflammatory mechanisms in hypertension.Nature reviews. Cardiology · 2024
    Review
  19. Article
  20. Article

20 more citing papers are in PubMed but not listed here.

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

13 authors at 3 institutions in 2 countries.

Allison E NorlanderDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, USA.
Mohamed A SalehDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Arvind K PandeyDivision of Cardiology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Hana A ItaniDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Jing WuDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, USA.
Liang XiaoDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Jooeun KangDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, USA.
Bethany L DaleDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, USA.
Slavina B GolevaDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, USA.
Fanny LaroumanieDivision of Clinical Pharmacology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Liping DuVanderbilt Center for Quantitative Sciences, Vanderbilt University School of Medicine, Nashville, Tennessee, USA.
David G HarrisonDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, USA.
Meena S MadhurDepartment of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, Tennessee, USA.
Vanderbilt University · USVanderbilt University Medical Center · USMansoura University · EG

Funding

CLINICAL PHARMACOLOGY TRAINING PROGRAMT32GM007569 · NIGMS · VANDERBILT UNIVERSITY MEDICAL CENTER · PI Bjorn C Knollmann · 1985 to 2026
$12.4M
Immunobiology of Blood and Vascular Systems Training ProgramT32HL069765 · NHLBI · VANDERBILT UNIVERSITY · PI HAWIGER, JACK J · 2002 to 2016
$6.5M
REGULATION OF VASCULAR FUNCTION BY THE ENDOTHELIUMR01HL039006 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRISON, DAVID G · 1987 to 2017
$5.5M
Immunophenotyping of Human Hypertension Using Single Cell Multiplex Mass Cytometry to Identify Novel Therapeutic TargetsDP2HL137166 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MADHUR, MEENAKSHI SWAMINATHAN · 2016 to 2021
$2.8M
The Role of The T Cell In The Genesis of Hypertension R01HL125865 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HARRISON, DAVID G · 2015 to 2017
$1.2M
Diverse Roles of Interleukin 17 Isoforms in the Pathogenesis of HypertensionK08HL121671 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI MADHUR, MEENAKSHI SWAMINATHAN · 2014 to 2018
$723k
The Effect of Salt on T Cell Function in HypertensionF31HL127986 · NHLBI · VANDERBILT UNIVERSITY · PI NORLANDER, ALLISON ELIZABETH · 2015 to 2016
$46k
NHLBI NIH HHS DP2 HL137166NHLBI NIH HHS F31 HL127986NHLBI NIH HHS K08 HL121671NHLBI NIH HHS R01 HL039006NHLBI NIH HHS R01 HL125865NHLBI NIH HHS T32 HL069765NIGMS NIH HHS T32 GM007569
6 · The paper itself

Abstract

We previously showed that angiotensin II (Ang II) increases T cell production of IL-17A, and that mice deficient in IL-17A have blunted hypertension and attenuated renal and vascular dysfunction. It was recently shown that salt enhances IL-17A production from CD4+ T cells via a serum- and glucocorticoid-regulated kinase 1-dependent (SGK1-dependent) pathway. Thus, we tested the hypothesis that SGK1 signaling in T cells promotes hypertension and contributes to end-organ damage. We show that loss of T cell SGK1 results in a blunted hypertensive response to Ang II infusion by 25 mmHg. Importantly, renal and vascular inflammation is abrogated in these mice compared with control mice. Furthermore, mice lacking T cell SGK1 are protected from Ang II-induced endothelial dysfunction and renal injury. Loss of T cell SGK1 also blunts blood pressure and vascular inflammation in response to deoxycorticosterone acetate-salt (DOCA-salt) hypertension. Finally, we demonstrate that the Na+-K+-2Cl- cotransporter 1 (NKCC1) is upregulated in Th17 cells and is necessary for the salt-induced increase in SGK1 and the IL-23 receptor. These studies demonstrate that T cell SGK1 and NKCC1 may be novel therapeutic targets for the treatment of hypertension and identify a potentially new mechanism by which salt contributes to hypertension.

Indexed as

Adaptive immunityCardiologyCardiovascular diseaseHypertensionInflammation

Identifiers

PMID28679951
PMCPMC5499362
OpenAlexW2730175149

What OpenQuestion holds

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Registered trials

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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.