Evidence map›Paper›PMID 18666097›Full record

ArticleThe Journal of pathology2008

Tight junction composition is altered in the epithelium of polycystic kidneys.

A S L Yu, S A Kanzawa, A Usorov, I S Lantinga-van Leeuwen, D J M Peters

Abstract read
In one paragraph

Article in The Journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

24 citing papers in PubMed, 35 citations in OpenAlex.

  1. Tight junction structure, assembly and (dys)function.Nature reviews. Molecular cell biology · 2026
    Review
  2. Article
  3. Intestinal barrier function declines during polycystic kidney disease progression.American journal of physiology. Renal physiology · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. VIP17/MAL expression modulates epithelial cyst formation and ciliogenesis.American journal of physiology. Cell physiology · 2012
    Article
  19. Dose-dependent effects of sirolimus on mTOR signaling and polycystic kidney disease.Journal of the American Society of Nephrology : JASN · 2012
    Article
  20. Ouabain modulates ciliogenesis in epithelial cells.Proceedings of the National Academy of Sciences of the United States of America · 2011
    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

5 authors at 2 institutions in 2 countries.

A S L YuDivision of Nephrology, Department of Medicine, University of Southern California Keck School of Medicine, Los Angeles, California 90089, USA. alanyu@usc.edu
S A Kanzawa
A Usorov
I S Lantinga-van Leeuwen
D J M Peters
University of Southern California · USLeiden University Medical Center · NL

Funding

USC RESEARCH CENTER FOR LIVER DISEASES: PILOT PROGRAMSP30DK048522 · NIDDK · UNIVERSITY OF SOUTHERN CALIFORNIA · PI KAPLOWITZ, NEIL · 1995 to 2020
$21.8M
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 DK48522NIDDK NIH HHS P30 DK048522NIDDK NIH HHS R01 DK062283
6 · The paper itself

Abstract

Kidney cysts in autosomal dominant polycystic kidney disease (ADPKD) undergo progressive enlargement together with luminal fluid secretion. This involves active, uphill transcellular Cl(-) transport which drives passive Na(+) and water secretion. Implicit in this mechanism is the assumption that the paracellular permeability of the cyst epithelium to Cl(-) must be very low. Claudins are tight junction (TJ) transmembrane proteins that determine the ion selectivity of paracellular barriers. The aim of this study was to determine the expression and localization of claudins within renal cysts in a mouse hypomorphic model of ADPKD and in human patients. We found that the majority of cysts were of collecting duct origin. Claudins normally expressed in collecting duct (3, 4, 7, 8, and 10) were found in small cysts. However, only claudin-7 persisted at substantive levels in the dedifferentiated epithelium of large, presumably late-stage cysts, where it was localized both at the TJ and basolaterally. The constitutively expressed TJ proteins, ZO-1 and occludin, were also abundantly expressed and correctly localized, suggesting that the basic infrastructure of the TJ is preserved. A previous study suggested that claudin-7 may function as a paracellular Cl(-) barrier. We postulate that the role of claudin-7 in ADPKD is to seal the paracellular route in Cl(-)-secreting cyst epithelium, preventing backleak of Cl(-), and that it thereby plays a permissive role in fluid secretion and cyst growth.

Indexed as

AnimalsEpithelial CellsHumansKidneyMembrane ProteinsMicePolycystic Kidney, Autosomal DominantTight JunctionsTumor Cells, CulturedMembrane Proteins

Identifiers

PMID18666097
PMCPMC2614395
OpenAlexW2041508753

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.