Evidence map›Paper›PMID 19349364›Full record

ArticleThe American journal of pathology2009

HIF-prolyl hydroxylases in the rat kidney: physiologic expression patterns and regulation in acute kidney injury.

Johannes Schödel, Bernd Klanke, Alexander Weidemann, Björn Buchholz, Wanja Bernhardt, Marko Bertog, Kerstin Amann, Christoph Korbmacher, Michael Wiesener, Christina Warnecke and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.

  1. Pooled it
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  13. Molecular regulation and function of FoxO3 in chronic kidney disease.Current opinion in nephrology and hypertension · 2020
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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

13 authors at 5 institutions in 4 countries.

Johannes SchödelDepartment of Nephrology and Hypertension, Friedrich-Alexander-University Erlangen-Nuremberg,Erlangen, Germany.
Bernd Klanke
Alexander Weidemann
Björn Buchholz
Wanja Bernhardt
Marko Bertog
Kerstin Amann
Christoph Korbmacher
Michael Wiesener
Christina Warnecke
Armin Kurtz
Kai-Uwe Eckardt
Carsten Willam
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEInstitut de Biologie Moléculaire et Cellulaire · FRCellular Research (United States) · USResearch Institute of Radiology · BYUniversity of Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hypoxia-inducible transcription factors (HIFs) play important roles in the response of the kidney to systemic and regional hypoxia. Degradation of HIFs is mediated by three oxygen-dependent HIF-prolyl hydroxylases (PHDs), which have partially overlapping characteristics. Although PHD inhibitors, which can induce HIFs in the presence of oxygen, are already in clinical development, little is known about the expression and regulation of these enzymes in the kidney. Therefore, we investigated the expression levels of the three PHDs in both isolated tubular cells and rat kidneys. All three PHDs were present in the kidney and were expressed predominantly in three different cell populations: (a) in distal convoluted tubules and collecting ducts (PHD1,2,3), (b) in glomerular podocytes (PHD1,3), and (c) in interstitial fibroblasts (PHD1,3). Higher levels of PHDs were found in tubular segments of the inner medulla where oxygen tensions are known to be physiologically low. PHD expression levels were unchanged in HIF-positive tubular and interstitial cells after induction by systemic hypoxia. In rat models of acute renal injury, changes in PHD expression levels were variable; while cisplatin and ischemia/reperfusion led to significant decreases in PHD2 and 3 expression levels, no changes were seen in a model of contrast media-induced nephropathy. These results implicate the non-uniform expression of HIF-regulating enzymes that modify the hypoxic response in the kidney under both regional and temporal conditions.

Indexed as

Acute Kidney InjuryAnimalsAntineoplastic AgentsBlotting, WesternCisplatinContrast MediaDNA-Binding ProteinsFibroblastsGene Expression Regulation, EnzymologicHomeodomain ProteinsHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Inducible Factor-Proline DioxygenasesImmediate-Early ProteinsImmunoenzyme TechniquesIschemiaKidneyAntineoplastic AgentsCisplatinContrast MediaDNA-Binding ProteinsEgln1 protein, ratEgln3 protein, ratHif1a protein, ratHomeodomain ProteinsHypoxia-Inducible Factor 1, alpha SubunitHypoxia-Inducible Factor-Proline DioxygenasesImmediate-Early ProteinsOxygenProcollagen-Proline DioxygenaseRNA, MessengerUncx protein, rat

Identifiers

PMID19349364
PMCPMC2671255
OpenAlexW140602058

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.