Evidence map›Paper›PMID 17322369›Full record

ArticleThe American journal of pathology2007

Involvement of hypoxia-inducible transcription factors in polycystic kidney disease.

Wanja Michael Bernhardt, Michael Sean Wiesener, Alexander Weidemann, Roland Schmitt, Wilko Weichert, Philipp Lechler, Valentina Campean, Albert Chee Meng Ong, Carsten Willam, Norbert Gretz and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 1 pooled it
4.0field-weighted citation impact, top 6% 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

59 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

  1. Guideline
  2. HIF-Regulated Pannexin-1 Channel Drives Luminal ATP Accumulation in Kidney Cysts.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Crosstalk between glomeruli and tubules.Nature reviews. Nephrology · 2025
    Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Review
  16. Article
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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

11 authors at 4 institutions in 2 countries.

Wanja Michael BernhardtDepartment of Nephrology and Hypertension, Friedrich-Alexander-University, Krankenhausstrasse 12, D-91054 Erlangen, Germany. wanja.bernhardt@med4.imed.uni-erlangen.de
Michael Sean Wiesener
Alexander Weidemann
Roland Schmitt
Wilko Weichert
Philipp Lechler
Valentina Campean
Albert Chee Meng Ong
Carsten Willam
Norbert Gretz
Kai-Uwe Eckardt
Friedrich-Alexander-Universität Erlangen-Nürnberg · DECharité - Universitätsmedizin Berlin · DEUniversity Medical Centre Mannheim · DEUniversity of Sheffield · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In polycystic kidney disease (PKD), erythropoietin (EPO) production and interstitial vascularization are increased compared with other kidney diseases. EPO and several angiogenic factors are controlled by hypoxia-inducible transcription factors (HIFs), which are composed of a constitutive beta-subunit and two alternative alpha-subunits (HIF-1alpha, HIF-2alpha). We hypothesized that cyst expansion may result in pericystic hypoxia and consecutive up-regulation of HIF and thus examined the expression of HIF-alpha and HIF target genes in human PKD and in a rodent PKD model. HIF-1alpha and HIF-2alpha were found to be up-regulated in cyst epithelium and cells of cyst walls, respectively. The distinct expression pattern of the HIF-alpha isoforms closely resembles the respective pattern in normal kidneys under systemic hypoxia. Pimonidazole staining, a marker for tissue hypoxia, confirmed the existence of regional hypoxia in polycystic kidneys. Immunohistochemistry for selected target genes implicated a role for HIF-1alpha in vascular endothelial growth factor and Glut-1 activation and HIF-2alpha in endoglin and EPO stimulation. Polycystin-deficient cells showed physiological, oxygen-dependent HIF-alpha modulation, excluding a direct influence of polycystin deficiency on HIF-alpha regulation. In conclusion, HIF accumulation in human and rat PKD seems to be responsible for increased EPO production and pericystic hypervascularity and may have an impact on progression of PKD.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCell HypoxiaErythropoietinFemaleGene ExpressionGlucose Transporter Type 1Heme Oxygenase-1HumansImmunoblottingImmunohistochemistryMaleMiddle AgedPolycystic Kidney DiseasesRatsTRPP Cation ChannelsBasic Helix-Loop-Helix ProteinsErythropoietinGlucose Transporter Type 1Heme Oxygenase-1HMOX1 protein, humanTRPP Cation ChannelsVascular Endothelial Growth Factor A

Identifiers

PMID17322369
PMCPMC1864863
OpenAlexW2120923776

What OpenQuestion holds

Textmetadata
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.