Evidence map›Paper›PMID 27871310›Full record

ArticleHuman genomics2016

Transcriptome analysis reveals manifold mechanisms of cyst development in ADPKD.

Rita M C de Almeida, Sherry G Clendenon, William G Richards, Michael Boedigheimer, Michael Damore, Sandro Rossetti, Peter C Harris, Britney-Shea Herbert, Wei Min Xu, Angela Wandinger-Ness and 3 more

Open access · goldAbstract read
In one paragraph

Article in Human genomics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

25 citing papers in PubMed, 33 citations in OpenAlex.

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  13. Clinical, histopathologic and molecular features of idiopathic and diabetic nodular mesangial sclerosis in humans.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2021
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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 7 institutions in 2 countries.

Rita M C de AlmeidaBiocomplexity Institute and Department of Physics, Indiana University, Bloomington, IN, 47405, USA.
Sherry G ClendenonBiocomplexity Institute and Department of Intelligent Systems Engineering, Indiana University, Bloomington, IN, 47405, USA.
William G RichardsAMGEN Inc., One Amgen Center Drive, Thousand Oaks, CA, 91320-1799, USA.
Michael BoedigheimerAMGEN Inc., One Amgen Center Drive, Thousand Oaks, CA, 91320-1799, USA.
Michael DamoreAMGEN Inc., One Amgen Center Drive, Thousand Oaks, CA, 91320-1799, USA.
Sandro RossettiDivision of Nephrology, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA.
Peter C HarrisDivision of Nephrology, Mayo Clinic, 200 First Street SW, Rochester, MN, 55905, USA.
Britney-Shea HerbertDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Wei Min XuDivision of Nephrology, Department of Medicine, Richard Roudebush VAMC and Indiana University School of Medicine, Indianapolis, IN, 46202, USA.
Angela Wandinger-NessDepartment of Pathology MSC08-4640 and Cancer Research and Treatment Center, University of New Mexico Health Sciences Center, Albuquerque, NM, 87131, USA.
Heather H WardDivision of Nephrology, Department of Medicine, University of New Mexico Health Sciences Center, Albuquerque, NM, 87131, USA.
James A GlazierBiocomplexity Institute and Department of Intelligent Systems Engineering, Indiana University, Bloomington, IN, 47405, USA.
Robert L BacallaoDivision of Nephrology, Department of Medicine, Richard Roudebush VAMC and Indiana University School of Medicine, Indianapolis, IN, 46202, USA. rbacalla@iupui.edu.
Amgen (United States) · USIndiana University Bloomington · USMayo Clinic · USRichard L. Roudebush VA Medical Center · USUniversity of New Mexico · USIndiana University School of MedicineUniversidade Federal do Rio Grande do Sul · BR

Funding

WOMEN'S CANCERS RESEARCH PROGRAMP30CA118100 · NCI · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI Yolanda Sanchez · 2005 to 2026
$57.1M
PROBE DELIVERY COREP30DK079312 · NIDDK · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI MOLITORIS, BRUCE A · 2007 to 2021
$17.1M
Pilot and FeasibilityP30DK090728 · NIDDK · MAYO CLINIC ROCHESTER · PI TORRES, VICENTE E · 2010 to 2019
$11.8M
MSM - Multiscale Studies of Segmentation in Vertebrate *R01GM076692 · NIGMS · TRUSTEES OF INDIANA UNIVERSITY · PI GLAZIER, JAMES ALEXANDER, STERN, CLAUDIO D · 2005 to 2015
$5.5M
Development and Improvement of Tissue Simulation ToolkitR01GM077138 · NIGMS · TRUSTEES OF INDIANA UNIVERSITY · PI D'SOUZA, ROSHAN M, GLAZIER, JAMES ALEXANDER · 2007 to 2015
$4.0M
Pathologic Mechanisms of Polycystic Kidney DiseaseR01DK050141 · NIDDK · UNIVERSITY OF NEW MEXICO · PI WANDINGER-NESS, ANGELA · 1995 to 2010
$2.7M
Targeting Fibrosis in Polycystic Kidney DiseaseK01DK097206 · NIDDK · UNIVERSITY OF WASHINGTON · PI WARD, HEATHER HILARY · 2014 to 2018
$600k
Endogenous Mitochondria Resistance to Acute Kidney InjuryI01BX001736 · VA · RLR VA MEDICAL CENTER · PI BACALLAO, ROBERT L · 2015 to 2018
–
BLRD VA I01 BX001736NCI NIH HHS P30 CA118100NIDDK NIH HHS K01 DK097206NIDDK NIH HHS P30 DK079312NIDDK NIH HHS P30 DK090728NIDDK NIH HHS R01 DK050141NIGMS NIH HHS R01 GM076692NIGMS NIH HHS R01 GM077138
6 · The paper itself

Abstract

backgroundAutosomal dominant polycystic kidney disease (ADPKD) causes progressive loss of renal function in adults as a consequence of the accumulation of cysts. ADPKD is the most common genetic cause of end-stage renal disease. Mutations in polycystin-1 occur in 87% of cases of ADPKD and mutations in polycystin-2 are found in 12% of ADPKD patients. The complexity of ADPKD has hampered efforts to identify the mechanisms underlying its pathogenesis. No current FDA (Federal Drug Administration)-approved therapies ameliorate ADPKD progression.

resultsWe used the de Almeida laboratory's sensitive new transcriptogram method for whole-genome gene expression data analysis to analyze microarray data from cell lines developed from cell isolates of normal kidney and of both non-cystic nephrons and cysts from the kidney of a patient with ADPKD. We compared results obtained using standard Ingenuity Volcano plot analysis, Gene Set Enrichment Analysis (GSEA) and transcriptogram analysis. Transcriptogram analysis confirmed the findings of Ingenuity, GSEA, and published analysis of ADPKD kidney data and also identified multiple new expression changes in KEGG (Kyoto Encyclopedia of Genes and Genomes) pathways related to cell growth, cell death, genetic information processing, nucleotide metabolism, signal transduction, immune response, response to stimulus, cellular processes, ion homeostasis and transport and cofactors, vitamins, amino acids, energy, carbohydrates, drugs, lipids, and glycans. Transcriptogram analysis also provides significance metrics which allow us to prioritize further study of these pathways.

conclusionsTranscriptogram analysis identifies novel pathways altered in ADPKD, providing new avenues to identify both ADPKD's mechanisms of pathogenesis and pharmaceutical targets to ameliorate the progression of the disease.

Indexed as

TranscriptomeAdultCase-Control StudiesCell LineGene Expression ProfilingGene OntologyHumansMaleMetabolic Networks and PathwaysMiddle AgedPolycystic Kidney, Autosomal DominantTRPP Cation ChannelsTRPP Cation ChannelsAutosomal dominant polycystic kidney diseaseBioinformaticsCystic kidney diseaseKidneyPathway identificationTranscriptogram

Identifiers

PMID27871310
PMCPMC5117508
OpenAlexW2554031258

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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.