SynthesisPloS one2012
Meta-analysis derived (MAD) transcriptome of psoriasis defines the "core" pathogenesis of disease.
Synthesis in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 5 of them syntheses that pooled it.
What it found
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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.
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.
Who cites it
94 citing papers in PubMed, 5 syntheses or guidelines pooled it.
- A shared tissue transcriptome signature and pathways in psoriasis and ulcerative colitis.Scientific reports · 2022Pooled it
- Pooled it
- Cross-Disease Transcriptomics: Unique IL-17A Signaling in Psoriasis Lesions and an Autoimmune PBMC Signature.The Journal of investigative dermatology · 2016Pooled it
- Increased expression of interleukin-17 pathway genes in nonlesional skin of moderate-to-severe psoriasis vulgaris.The British journal of dermatology · 2016Pooled it
- Meta-analysis derived atopic dermatitis (MADAD) transcriptome defines a robust AD signature highlighting the involvement of atherosclerosis and lipid metabolism pathways.BMC medical genomics · 2015Pooled it
- Icotrokinra induces early and sustained pharmacodynamic responses in phase IIb study of patients with moderate-to-severe psoriasis.JCI insight · 2025Trial
- A Randomized, Placebo-Controlled Study of SRT2104, a SIRT1 Activator, in Patients with Moderate to Severe Psoriasis.PloS one · 2015Trial
- Modulation of epidermal transcription circuits in psoriasis: new links between inflammation and hyperproliferation.PloS one · 2013Trial
- Adiponectin Inhibits AURKA to Suppress Inflammation in TNF-α-induced Keratinocytes and Attenuates Psoriatic Dermatitis in Mice.Immunity, inflammation and disease · 2026Article
- A Novel Chronic Psoriasis Mouse Model via Optimized Imiquimod Dosing and Machine Learning Evaluation.Journal of inflammation research · 2026Article
- Meta-Analysis of Gene Expression Reveals the Core Transcriptomic Profile of Lesional Scalp in Alopecia Areata.Dermatology and therapy · 2025Review
- Epidermal proteomics demonstrates Elafin as a psoriasis-specific biomarker and highlights increased anti-inflammatory activity around psoriatic plaques.Journal of the European Academy of Dermatology and Venereology : JEADV · 2025Article
- An unbiased tissue transcriptome analysis identifies potential markers for skin phenotypes and therapeutic responses in atopic dermatitis.Nature communications · 2025Article
- Impact of Treatment Interruption on the Effectiveness of Interleukin (IL)-17A Inhibitors in Plaque Psoriasis: A Retrospective Analysis.International journal of general medicine · 2025Article
- Differential Pharmacodynamic Effects on Psoriatic Biomarkers by Guselkumab Versus Secukinumab Correlate with Long-Term Efficacy: An ECLIPSE Substudy.JID innovations : skin science from molecules to population health · 2024Article
- Guselkumab Reduces Disease- and Mechanism-Related Biomarkers More Than Adalimumab in Patients with Psoriasis: A VOYAGE 1 Substudy.JID innovations : skin science from molecules to population health · 2024Article
- Review
- Gram-negative anaerobes elicit a robust keratinocytes immune response with potential insights into HS pathogenesis.Experimental dermatology · 2024Article
- Article
- Evaluation ofMediators of inflammation · 2024Article
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
The cause of psoriasis, a common chronic inflammatory skin disease, is not fully understood. Microarray experiments have been widely used in recent years to identify genes associated with psoriasis pathology, by comparing expression levels of lesional (LS) with adjacent non-lesional (NL) skin. It is commonly observed that the differentially expressed genes (DEGs) differ greatly across experiments, due to variations introduced in the microarray experiment pipeline. Therefore, a statistically based meta-analytic approach, which combines the results of individual studies, is warranted. In this study, a meta-analysis was conducted on 5 microarray data sets, including 193 LS and NL pairs. We termed this the Meta-Analysis Derived (MAD) transcriptome. In "MAD-5" transcriptome, 677 genes were up-regulated and 443 were down-regulated in LS skin compared to NL skin. This represents a much larger set than the intersection of DEGs of these 5 studies, which consisted of 100 DEGs. We also analyzed 3 of the studies conducted on the Affymetrix hgu133plus2 chips and found a greater number of DEGs (1084 up- and 748 down-regulated). Top canonical pathways over-represented in the MAD transcriptome include Atherosclerosis Signaling and Fatty Acid Metabolism, while several "new" genes identified are involved in Cardiovascular Development and Lipid Metabolism. These findings highlight the relationship between psoriasis and systemic manifestations such as the metabolic syndrome and cardiovascular disease. Then, the Meta Threshold Gradient Descent Regularization (MTGDR) algorithm was used to select potential markers distinguishing LS and NL skin. The resulting set (20 genes) contained many genes that were part of the residual disease genomic profile (RDGP) or "molecular scar" after successful treatment, and also genes subject to differential methylation in LS tissues. To conclude, this MAD transcriptome yielded a reference list of reliable psoriasis DEGs, and represents a robust pool of candidates for further discovery of pathogenesis and treatment evaluation.
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Registered trials
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.