Evidence map›Paper›PMID 18795318›Full record

ReviewPflugers Archiv : European journal of physiology2009

Function and regulation of claudins in the thick ascending limb of Henle.

Dorothee Günzel, Alan S L Yu

Abstract readReview
In one paragraph

Review in Pflugers Archiv : European journal of physiology, 2009. 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
3.4field-weighted citation impact, top 9% 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, 56 citations in OpenAlex.

  1. Actin cytoskeleton and associated myosin motors within the renal epithelium.American journal of physiology. Renal physiology · 2024
    Review
  2. Article
  3. Renal cell markers: lighthouses for managing renal diseases.American journal of physiology. Renal physiology · 2021
    Article
  4. Review
  5. Review
  6. A Novel Hypokalemic-Alkalotic Salt-Losing Tubulopathy in Patients withJournal of the American Society of Nephrology : JASN · 2017
    Article
  7. AVP dynamically increases paracellular NaPflugers Archiv : European journal of physiology · 2017
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Claudins in lung diseases.Respiratory research · 2011
    Review
  16. Renal, ocular, and neuromuscular involvements in patients with CLDN19 mutations.Clinical journal of the American Society of Nephrology : CJASN · 2011
    Article
  17. Differential expression of claudin tight junction proteins in the human cortical nephron.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2010
    Article
  18. A molecularly guided tour along the nephron.Pflugers Archiv : European journal of physiology · 2009
    Article
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

2 authors at 2 institutions in 2 countries.

Dorothee GünzelDepartment of Clinical Physiology, Charité, Campus Benjamin Franklin, Berlin, Germany.
Alan S L Yu
Charité - Universitätsmedizin Berlin · DEUniversity of Southern California · US

Funding

Expression, function and regulation of renal claudinsR01DK062283 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI YU, ALAN S · 2003 to 2010
$2.7M
NIDDK NIH HHS DK062283NIDDK NIH HHS R01 DK062283
6 · The paper itself

Abstract

The thick ascending limb (TAL) of Henle mediates transcellular reabsorption of NaCl while generating a lumen-positive voltage that drives passive paracellular reabsorption of divalent cations. Disturbance of paracellular reabsorption leads to Ca(2+) and Mg(2+) wasting in patients with the rare inherited disorder of familial hypercalciuric hypomagnesemia with nephrocalcinosis (FHHNC). Recent work has shown that the claudin family of tight junction proteins form paracellular pores and determine the ion selectivity of paracellular permeability. Importantly, FHHNC has been found to be caused by mutations in two of these genes, claudin-16 and claudin-19, and mice with knockdown of claudin-16 reproduce many of the features of FHHNC. Here, we review the physiology of TAL ion transport, present the current view of the role and mechanism of claudins in determining paracellular permeability, and discuss the possible pathogenic mechanisms responsible for FHHNC.

Indexed as

AnimalsBartter SyndromeBiological Transport, ActiveCalciumClaudinsGitelman SyndromeHumansLoop of HenleMagnesiumMembrane ProteinsNephrocalcinosisReceptors, Calcium-SensingTight JunctionsCalciumCASR protein, humanclaudin 16ClaudinsCldn19 protein, mouseMagnesiumMembrane ProteinsReceptors, Calcium-Sensing

Identifiers

PMID18795318
PMCPMC2666100
OpenAlexW2081557881

What OpenQuestion holds

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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.