Evidence map›Paper›PMID 27815594›Full record

ReviewCellular and molecular life sciences : CMLS2017

WNK signalling pathways in blood pressure regulation.

Meena Murthy, Thimo Kurz, Kevin M O'Shaughnessy

Open access · hybridAbstract readReview
In one paragraph

Review in Cellular and molecular life sciences : CMLS, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

28 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
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  15. Multifaceted roles of SARM1 in axon degeneration and signaling.Frontiers in cellular neuroscience · 2022
    Review
  16. [A Case of Pseudohypoaldosteronism Type Ⅱ (PHA2) Caused by a Novel Mutation ofSichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021
    Article
  17. Article
  18. Review
  19. Intracellular ClInternational journal of molecular sciences · 2020
    Review
  20. 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

3 authors at 2 institutions in 1 country.

Meena MurthyDivision of Experimental Medicine and Immunotherapeutics, Department of Medicine, University of Cambridge, Cambridge, CB2 2QQ, UK.
Thimo KurzInstitute of Molecular Cell and Systems Biology, University of Glasgow, Davidson Building, Glasgow, G12 8QQ, Scotland, UK.
Kevin M O'ShaughnessyDivision of Experimental Medicine and Immunotherapeutics, Department of Medicine, University of Cambridge, Cambridge, CB2 2QQ, UK. kmo22@medschl.cam.ac.uk.ORCID 0000-0002-1476-7566
University of Cambridge · GBUniversity of Glasgow · GB

Funding

British Heart Foundation PG/13/89/30577Medical Research Council MC_UU_12016/7
6 · The paper itself

Abstract

Hypertension (high blood pressure) is a major public health problem affecting more than a billion people worldwide with complications, including stroke, heart failure and kidney failure. The regulation of blood pressure is multifactorial reflecting genetic susceptibility, in utero environment and external factors such as obesity and salt intake. In keeping with Arthur Guyton's hypothesis, the kidney plays a key role in blood pressure control and data from clinical studies; physiology and genetics have shown that hypertension is driven a failure of the kidney to excrete excess salt at normal levels of blood pressure. There is a number of rare Mendelian blood pressure syndromes, which have shed light on the molecular mechanisms involved in dysregulated ion transport in the distal kidney. One in particular is Familial hyperkalemic hypertension (FHHt), an autosomal dominant monogenic form of hypertension characterised by high blood pressure, hyperkalemia, hyperchloremic metabolic acidosis, and hypercalciuria. The clinical signs of FHHt are treated by low doses of thiazide diuretic, and it mirrors Gitelman syndrome which features the inverse phenotype of hypotension, hypokalemic metabolic alkalosis, and hypocalciuria. Gitelman syndrome is caused by loss of function mutations in the thiazide-sensitive Na/Cl cotransporter (NCC); however, FHHt patients do not have mutations in the SCL12A3 locus encoding NCC. Instead, mutations have been identified in genes that have revealed a key signalling pathway that regulates NCC and several other key transporters and ion channels in the kidney that are critical for BP regulation. This is the WNK kinase signalling pathway that is the subject of this review.

Indexed as

Signal TransductionAnimalsBlood PressureCullin ProteinsHumansHypertensionNeovascularization, PhysiologicProtein Serine-Threonine KinasesPseudohypoaldosteronismReceptors, DrugSodium Chloride SymportersSodium-Potassium-Chloride SymportersCullin ProteinsProtein Serine-Threonine KinasesReceptors, DrugSodium Chloride SymportersSodium-Potassium-Chloride Symportersthiazide receptorHyperkalemiaHypertensionNCCProteasomeSPAK/OSR1 phosphorylationUbiquitin-E3 ligase complexWNK kinases

Identifiers

PMID27815594
PMCPMC5346417
OpenAlexW2548645442

What OpenQuestion holds

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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.