Evidence map›Paper›PMID 27191348›Full record

ReviewCurrent opinion in nephrology and hypertension2016

Claudins and mineral metabolism.

Jianghui Hou

Open access · greenAbstract readReview
In one paragraph

Review in Current opinion in nephrology and hypertension, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Review
  6. Claudins in kidney health and disease.Kidney research and clinical practice · 2022
    Article
  7. Mutations inCanadian journal of kidney health and disease · 2022
    Article
  8. Review
  9. Tight junctions and their regulation by non-coding RNAs.International journal of biological sciences · 2021
    Review
  10. Article
  11. Review
  12. Renal CaInternational journal of molecular sciences · 2019
    Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. 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

1 author at 1 institution in 1 country.

Jianghui HouWashington University Renal Division, St. Louis, Missouri, USA.
Washington University in St. Louis · US

Funding

Washington University Center for Kidney Disease ResearchP30DK079333 · NIDDK · WASHINGTON UNIVERSITY · PI HAMMERMAN, MARC RANDALL · 2007 to 2011
$5.1M
BIOCHEMICAL AND BIOPHYSICAL NATURE OF CLAUDIN-16 AND CLAUDIN-19 CHANNELSR01DK084059 · NIDDK · WASHINGTON UNIVERSITY · PI HOU, JIANGHUI · 2010 to 2018
$2.9M
NIDDK NIH HHS P30 DK079333NIDDK NIH HHS R01 DK084059
6 · The paper itself

Abstract

purpose of reviewThe tight junction conductance made of the claudin-based paracellular channel is important in the regulation of calcium and magnesium reabsorption in the kidney. This review describes recent findings of the structure, the function, and the physiologic regulation of claudin-14, claudin-16, and claudin-19 channels that through protein interactions confer calcium and magnesium permeability to the tight junction. RECENT

findingsMutations in two tight junction genes - claudin-16 and claudin-19 - cause the inherited renal disorder familial hypomagnesemia with hypercalciuria and nephrocalcinosis. A recent genome-wide association study has identified claudin-14 as a major risk gene of hypercalciuric nephrolithiasis. The crystal structure of claudin-19 has recently been resolved allowing the reconstruction of a claudin assembly model from cis-dimers made of claudin-16 and claudin-19 interaction. MicroRNAs have been identified as novel regulators of the claudin-14 gene. The microRNA-claudin-14 operon is directly regulated by the Ca sensing receptor gene in response to hypercalcemia. SUMMARY: The paracellular pathway in the kidney is particularly important for mineral metabolism. Three claudin proteins - claudin-14, claudin-16, and claudin-19 - contribute to the structure and function of this paracellular pathway. Genetic mutations and gene expression changes in these claudins may lead to alteration of the paracellular permeability to calcium and magnesium, ultimately affecting renal mineral metabolism.

Indexed as

CalciumClaudinsGenome-Wide Association StudyHumansHypercalciuriaKidneyMagnesiumMicroRNAsNephrocalcinosisNephrolithiasisReceptors, Calcium-SensingRenal Tubular Transport, Inborn ErrorsTight JunctionsCalciumclaudin 14claudin 16ClaudinsCLDN19 protein, humanMagnesiumMicroRNAsReceptors, Calcium-Sensing

Identifiers

PMID27191348
PMCPMC4891285
OpenAlexW2402261625

What OpenQuestion holds

Textmetadata
LicenceTDM
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.