Evidence map›Paper›PMID 34335565›Full record

ArticleFrontiers in immunology2021

Exploration of the Shared Gene Signatures and Molecular Mechanisms Between Systemic Lupus Erythematosus and Pulmonary Arterial Hypertension: Evidence From Transcriptome Data.

Menghui Yao, Chunyi Zhang, Congcong Gao, Qianqian Wang, Mengmeng Dai, Runzhi Yue, Wenbo Sun, Wenfang Liang, Zhaohui Zheng

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
10.9field-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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Menghui YaoDepartment of Rheumatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Chunyi ZhangDepartment of Rheumatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Congcong GaoDepartment of Rheumatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Qianqian WangDepartment of Rheumatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Mengmeng DaiDepartment of Rheumatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Runzhi YueDepartment of Rheumatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Wenbo SunDepartment of Rheumatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Wenfang LiangDepartment of Rheumatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Zhaohui ZhengDepartment of Rheumatology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
First Affiliated Hospital of Zhengzhou University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Systemic lupus erythematosus (SLE) is an autoimmune disease that can affect multiple systems. Pulmonary arterial hypertension (PAH) has a close linkage with SLE. However, the inter-relational mechanisms between them are still unclear. This article aimed to explore the shared gene signatures and potential molecular mechanisms in SLE and PAH. Methods: The microarray data of SLE and PAH in the Gene Expression Omnibus (GEO) database were downloaded. The Weighted Gene Co-Expression Network Analysis (WGCNA) was used to identify the co-expression modules related to SLE and PAH. The shared genes existing in the SLE and PAH were performed an enrichment analysis by ClueGO software, and their unique genes were also performed with biological processes analyses using the DAVID website. The results were validated in another cohort by differential gene analysis. Moreover, the common microRNAs (miRNAs) in SLE and PAH were obtained from the Human microRNA Disease Database (HMDD) and the target genes of whom were predicted through the miRTarbase. Finally, we constructed the common miRNAs-mRNAs network with the overlapped genes in target and shared genes. Results: Using WGCNA, four modules and one module were identified as the significant modules with SLE and PAH, respectively. A ClueGO enrichment analysis of shared genes reported that highly activated type I IFN response was a common feature in the pathophysiology of SLE and PAH. The results of differential analysis in another cohort were extremely similar to them. We also proposed a disease road model for the possible mechanism of PAH secondary to SLE according to the shared and unique gene signatures in SLE and PAH. The miRNA-mRNA network showed that hsa-miR-146a might regulate the shared IFN-induced genes, which might play an important role in PAH secondary to SLE. Conclusion: Our work firstly revealed the high IFN response in SLE patients might be a crucial susceptible factor for PAH and identified novel gene candidates that could be used as biomarkers or potential therapeutic targets.

Indexed as

Gene Expression RegulationTranscriptomeBiomarkersComputational BiologyDatabases, GeneticDisease SusceptibilityGene Expression ProfilingGene Regulatory NetworksHumansLupus Erythematosus, SystemicMicroRNAsModels, BiologicalPulmonary Arterial HypertensionRNA InterferenceRNA, MessengerBiomarkersMicroRNAsRNA, Messengerdifferential gene analysismiRNAs–mRNAspulmonary arterial hypertensionsystemic lupus erythematosustype I IFNWGCNA

Identifiers

PMID34335565
PMCPMC8320323
OpenAlexW3186605920

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.