Evidence map›Paper›PMID 20081107›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2010

Genomewide RNA expression profiling in lung identifies distinct signatures in idiopathic pulmonary arterial hypertension and secondary pulmonary hypertension.

Revathi Rajkumar, Kazuhisa Konishi, Thomas J Richards, David C Ishizawar, Andrew C Wiechert, Naftali Kaminski, Ferhaan Ahmad

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
128citing papers in PubMed, 4 pooled it
12.7field-weighted citation impact, top 1% 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

128 citing papers in PubMed, 4 syntheses or guidelines pooled it, 197 citations in OpenAlex.

  1. A Cross-Species and Sex-Specific Meta-Analysis of Transcriptomic Studies of Pulmonary Hypertension.American journal of respiratory cell and molecular biology · 2025
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  16. Dissecting the lung transcriptome of pulmonary fibrosis-associated pulmonary hypertension.American journal of physiology. Lung cellular and molecular physiology · 2024
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68 more citing papers are in PubMed but not listed here.

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

7 authors at 2 institutions in 2 countries.

Revathi RajkumarCardiovascular Institute, Univ. of Pittsburgh, PA 15213-2582, USA.
Kazuhisa Konishi
Thomas J Richards
David C Ishizawar
Andrew C Wiechert
Naftali Kaminski
Ferhaan Ahmad
Cardiovascular Institute Hospital · JPUniversity of Pittsburgh · US

Funding

UNIVERSITY OF PITTSBURGH CLINICAL AND TRANSLATIONAL SCIENCE INSTITUTE: BPCAUL1RR024153 · NCRR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI REIS, STEVEN E · 2006 to 2011
$73.9M
Molecular Phenotypes within and across disease boundaries in IPF and COPDR01HL095397 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAMINSKI, NAFTALI, SHAPIRO, STEVEN D · 2008 to 2011
$3.0M
Molecular Mechanisms of Pulmonary Hypertension in COPDR03HL095401 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI AHMAD, FERHAAN · 2009 to 2010
$152k
NCRR NIH HHS 5UL1 RR024153-02NHLBI NIH HHS HL095397NHLBI NIH HHS HL095401
6 · The paper itself

Abstract

Idiopathic pulmonary arterial hypertension (PAH) is a life-threatening condition characterized by pulmonary arteriolar remodeling. This investigation aimed to identify genes involved specifically in the pathogenesis of PAH and not other forms of pulmonary hypertension (PH). Using genomewide microarray analysis, we generated the largest data set to date of RNA expression profiles from lung tissue specimens from 1) 18 PAH subjects and 2) 8 subjects with PH secondary to idiopathic pulmonary fibrosis (IPF) and 3) 13 normal subjects. A molecular signature of 4,734 genes discriminated among these three cohorts. We identified significant novel biological changes that were likely to contribute to the pathogenesis of PAH, including regulation of actin-based motility, protein ubiquitination, and cAMP, transforming growth factor-beta, MAPK, estrogen receptor, nitric oxide, and PDGF signaling. Bone morphogenic protein receptor type II expression was downregulated, even in subjects without a mutation in this gene. Women with PAH had higher expression levels of estrogen receptor 1 than normal women. Real-time quantitative PCR confirmed differential expression of the following genes in PAH relative to both normal controls and PH secondary to IPF: a disintegrin-like and metalloprotease with thrombospondin type 1 motif 9, cell adhesion molecule with homology to L1CAM, cytochrome b(558) and beta-polypeptide, coagulation factor II receptor-like 3, A-myb myeloblastosis viral oncogene homolog 1, nuclear receptor coactivator 2, purinergic receptor P2Y, platelet factor 4, phospholamban, and tropomodulin 3. This study shows that PAH and PH secondary to IPF are characterized by distinct gene expression signatures, implying distinct pathophysiological mechanisms.

Indexed as

Gene Expression ProfilingAdultAgedBone Morphogenetic Protein Receptors, Type IICase-Control StudiesEstrogen Receptor alphaFemaleGenome, HumanHumansHypertension, PulmonaryIdiopathic Pulmonary FibrosisLungMaleMiddle AgedRNASignal TransductionBMPR2 protein, humanBone Morphogenetic Protein Receptors, Type IIESR1 protein, humanEstrogen Receptor alphaRNA

Identifiers

PMID20081107
PMCPMC2853417
OpenAlexW2098148891

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.