Evidence map›Paper›PMID 30642337›Full record

ArticleBMC systems biology2019

Multi-omics integration reveals molecular networks and regulators of psoriasis.

Yuqi Zhao, Deepali Jhamb, Le Shu, Douglas Arneson, Deepak K Rajpal, Xia Yang

Open access · diamondAbstract read
In one paragraph

Article in BMC systems biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 45 citations in OpenAlex.

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  7. Multi-Omics Research Strategies for Psoriasis and Atopic Dermatitis.International journal of molecular sciences · 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

6 authors at 3 institutions in 1 country.

Yuqi ZhaoDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Dr. East, Los Angeles, CA, 90095, USA.
Deepali JhambTarget Sciences, Computational Biology (US) GSK, 1250 South Collegeville Road, Collegeville, PA, 19426, USA.
Le ShuDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Dr. East, Los Angeles, CA, 90095, USA.
Douglas ArnesonDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Dr. East, Los Angeles, CA, 90095, USA.
Deepak K RajpalTarget Sciences, Computational Biology (US) GSK, 1250 South Collegeville Road, Collegeville, PA, 19426, USA. deepak.k.rajpal@gsk.com.
Xia YangDepartment of Integrative Biology and Physiology, University of California, Los Angeles, 610 Charles E. Young Dr. East, Los Angeles, CA, 90095, USA. xyang123@ucla.edu.
University of California, Los Angeles · USSouth College · USTarget (United States) · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPsoriasis is a complex multi-factorial disease, involving both genetic susceptibilities and environmental triggers. Genome-wide association studies (GWAS) and epigenome-wide association studies (EWAS) have been carried out to identify genetic and epigenetic variants that are associated with psoriasis. However, these loci cannot fully explain the disease pathogenesis.

methodsTo achieve a comprehensive mechanistic understanding of psoriasis, we conducted a systems biology study, integrating multi-omics datasets including GWAS, EWAS, tissue-specific transcriptome, expression quantitative trait loci (eQTLs), gene networks, and biological pathways to identify the key genes, processes, and networks that are genetically and epigenetically associated with psoriasis risk.

resultsThis integrative genomics study identified both well-characterized (e.g., the IL17 pathway in both GWAS and EWAS) and novel biological processes (e.g., the branched chain amino acid catabolism process in GWAS and the platelet and coagulation pathway in EWAS) involved in psoriasis. Finally, by utilizing tissue-specific gene regulatory networks, we unraveled the interactions among the psoriasis-associated genes and pathways in a tissue-specific manner and detected potential key regulatory genes in the psoriasis networks.

conclusionsThe integration and convergence of multi-omics signals provide deeper and comprehensive insights into the biological mechanisms associated with psoriasis susceptibility.

Indexed as

EpigenomicsGene Expression ProfilingGenome-Wide Association StudyGene Regulatory NetworksHumansOrgan SpecificityPsoriasisQuantitative Trait LociSystems BiologyEWASGWASIntegrative genomicsPsoriasisSystems biology

Identifiers

PMID30642337
PMCPMC6332659
OpenAlexW2912234274

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.