Evidence map›Paper›PMID 28819298›Full record

ArticleScientific reports2017

Transcriptome-based network analysis reveals renal cell type-specific dysregulation of hypoxia-associated transcripts.

Natallia Shved, Gregor Warsow, Felix Eichinger, David Hoogewijs, Simone Brandt, Peter Wild, Matthias Kretzler, Clemens D Cohen, Maja T Lindenmeyer

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 76 citations in OpenAlex.

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  14. Evolution of hypoxia and hypoxia-inducible factor asparaginyl hydroxylase regulation in chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
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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

9 authors at 5 institutions in 3 countries.

Natallia ShvedInstitute of Physiology and Division of Nephrology, University of Zurich, Zurich, Switzerland.
Gregor WarsowDepartment of Anatomy and Cell Biology, Universitätsmedizin Greifswald, Greifswald, Germany; Division of Theoretical Bioinformatics (B080), German Cancer Research Center (DKFZ), Heidelberg, Germany.
Felix EichingerDepartment of Medicine, University of Michigan, Ann Arbor, Michigan, USA.
David HoogewijsDepartment of Medicine/Physiology, University of Fribourg, Fribourg, Switzerland; Institute of Physiology, University of Zurich, Zurich, Switzerland.
Simone BrandtInstitute of Pathology and Molecular Pathology, University Hospital Zurich, Zurich, Switzerland.
Peter WildInstitute of Pathology and Molecular Pathology, University Hospital Zurich, Zurich, Switzerland.
Matthias KretzlerDepartment of Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Clemens D CohenInstitute of Physiology and Division of Nephrology, University of Zurich, Zurich, Switzerland.
Maja T LindenmeyerInstitute of Physiology and Division of Nephrology, University of Zurich, Zurich, Switzerland. maja.lindenmeyer@med.uni-muenchen.de.
University of Zurich · CHUniversity Hospital of Zurich · CHUniversity of Michigan–Ann Arbor · USGerman Cancer Research Center · DELudwig-Maximilians-Universität München · DE

Funding

University of Michigan O'Brien Kidney Translational Core CenterP30DK081943 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI PENNATHUR, SUBRAMANIAM · 2008 to 2022
$12.9M
NIDDK NIH HHS P30 DK081943
6 · The paper itself

Abstract

Accumulating evidence suggests that dysregulation of hypoxia-regulated transcriptional mechanisms is involved in development of chronic kidney diseases (CKD). However, it remains unclear how hypoxia-induced transcription factors (HIFs) and subsequent biological processes contribute to CKD development and progression. In our study, genome-wide expression profiles of more than 200 renal biopsies from patients with different CKD stages revealed significant correlation of HIF-target genes with eGFR in glomeruli and tubulointerstitium. These correlations were positive and negative and in part compartment-specific. Microarrays of proximal tubular cells and podocytes with stable HIF1α and/or HIF2α suppression displayed cell type-specific HIF1/HIF2-dependencies as well as dysregulation of several pathways. WGCNA analysis identified gene sets that were highly coregulated within modules. Characterization of the modules revealed common as well as cell group- and condition-specific pathways, GO-Terms and transcription factors. Gene expression analysis of the hypoxia-interconnected pathways in patients with different CKD stages revealed an increased dysregulation with loss of renal function. In conclusion, our data clearly point to a compartment- and cell type-specific dysregulation of hypoxia-associated gene transcripts and might help to improve the understanding of hypoxia, HIF dysregulation, and transcriptional program response in CKD.

Indexed as

Gene Regulatory NetworksTranscriptomeBasic Helix-Loop-Helix ProteinsCell HypoxiaCell LineCells, CulturedEndothelial PAS Domain-Containing Protein 1Gene Expression ProfilingGene OntologyHumansHypoxiaHypoxia-Inducible Factor 1, alpha SubunitKidneyKidney GlomerulusPodocytesRenal Insufficiency, ChronicBasic Helix-Loop-Helix ProteinsEndothelial PAS Domain-Containing Protein 1Hypoxia-Inducible Factor 1, alpha Subunit

Identifiers

PMID28819298
PMCPMC5561250
OpenAlexW2745104857

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.