Evidence map›Paper›PMID 26459294›Full record

SynthesisBMC medical genomics2015

Meta-analysis derived atopic dermatitis (MADAD) transcriptome defines a robust AD signature highlighting the involvement of atherosclerosis and lipid metabolism pathways.

David A Ewald, Dana Malajian, James G Krueger, Christopher T Workman, Tianjiao Wang, Suyan Tian, Thomas Litman, Emma Guttman-Yassky, Mayte Suárez-Fariñas

Abstract readMeta-Analysis
In one paragraph

Synthesis in BMC medical genomics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

61 citing papers in PubMed, 4 syntheses or guidelines pooled it.

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  20. A Bispecific, Tetravalent Antibody Targeting Inflammatory and Pruritogenic Pathways in Atopic Dermatitis.JID innovations : skin science from molecules to population health · 2024
    Article

1 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

9 authors.

David A EwaldThe Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA. ewald@cbs.dtu.dk.
Dana MalajianThe Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA. dana.malajian@gmail.com.
James G KruegerThe Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA. kruegej@rockefeller.edu.
Christopher T WorkmanCenter for Biological Sequence Analysis, Department of Systems Biology, Technical University of Denmark, Kgs. Lyngby, Denmark. workman@cbs.dtu.dk.
Tianjiao WangSchool of Life Science, Jilin University, 2699 Qianjin Street, Changchun, Jilin, 130012, China. jiaolx@qq.com.
Suyan TianSchool of Life Science, Jilin University, 2699 Qianjin Street, Changchun, Jilin, 130012, China. windytian@hotmail.com.
Thomas LitmanMolecular Biomedicine, LEO Pharma AS, Ballerup, Denmark. thomas.litman@leo-pharma.com.
Emma Guttman-YasskyThe Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA. eguttman@rockefeller.edu.
Mayte Suárez-FariñasThe Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY, USA. farinam@rockefeller.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtopic dermatitis (AD) is a common inflammatory skin disease with limited treatment options. Several microarray experiments have been conducted on lesional/LS and non-lesional/NL AD skin to develop a genomic disease phenotype. Although these experiments have shed light on disease pathology, inter-study comparisons reveal large differences in resulting sets of differentially expressed genes (DEGs), limiting the utility of direct comparisons across studies.

methodsWe carried out a meta-analysis combining 4 published AD datasets to define a robust disease profile, termed meta-analysis derived AD (MADAD) transcriptome.

resultsThis transcriptome enriches key AD pathways more than the individual studies, and associates AD with novel pathways, such as atherosclerosis signaling (IL-37, selectin E/SELE). We identified wide lipid abnormalities and, for the first time in vivo, correlated Th2 immune activation with downregulation of key epidermal lipids (FA2H, FAR2, ELOVL3), emphasizing the role of cytokines on the barrier disruption in AD. Key AD "classifier genes" discriminate lesional from nonlesional skin, and may evaluate therapeutic responses.

conclusionsOur meta-analysis provides novel and powerful insights into AD disease pathology, and reinforces the concept of AD as a systemic disease.

Indexed as

AtherosclerosisDermatitis, AtopicGene Expression ProfilingGene Regulatory NetworksHumansLipid MetabolismTh2 Cells

Identifiers

PMID26459294
PMCPMC4603338

What Socratic holds

Textmetadata
LicenceCC BY
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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 Socratic graph.