Evidence map›Paper›PMID 32860486›Full record

ArticleJournal of cellular and molecular medicine2020

Transcriptomic analysis identifies Toll-like and Nod-like pathways and necroptosis in pulmonary arterial hypertension.

Genfa Xiao, Wei Zhuang, Tingjun Wang, Guili Lian, Li Luo, Chaoyi Ye, Huajun Wang, Liangdi Xie

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
6.5field-weighted citation impact, top 2% 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

40 citing papers in PubMed, 71 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

8 authors at 1 institution in 1 country.

Genfa XiaoDepartment of Geriatrics, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, People's Republic of China.ORCID 0000-0003-1697-5905
Wei ZhuangFujian Hypertension Research Institute, The First Affiliated Hospital of Fujian Medical University, People's Republic of China.ORCID 0000-0002-9972-8717
Tingjun WangDepartment of Geriatrics, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, People's Republic of China.ORCID 0000-0002-5214-9590
Guili LianFujian Hypertension Research Institute, The First Affiliated Hospital of Fujian Medical University, People's Republic of China.ORCID 0000-0001-5909-3991
Li LuoDepartment of Geriatrics, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, People's Republic of China.
Chaoyi YeFujian Hypertension Research Institute, The First Affiliated Hospital of Fujian Medical University, People's Republic of China.
Huajun WangFujian Hypertension Research Institute, The First Affiliated Hospital of Fujian Medical University, People's Republic of China.
Liangdi XieDepartment of Geriatrics, The First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, People's Republic of China.ORCID 0000-0001-5544-3149
Fujian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation and immunity play a causal role in the pathogenesis of pulmonary vascular remodelling and pulmonary arterial hypertension (PAH). However, the pathways and mechanisms by which inflammation and immunity contribute to pulmonary vascular remodelling remain unknown. RNA sequencing was used to analyse the transcriptome in control and rats injected with monocrotaline (MCT) for various weeks. Using the transcriptional profiling of MCT-induced PAH coupled with bioinformatics analysis, we clustered the differentially expressed genes (DEGs) and chose the increased expression patterns associated with inflammatory and immune response. We found the enrichment of Toll-like receptor (TLR) and Nod-like receptor (NLR) pathways and identified NF-κB-mediated inflammatory and immune profiling in MCT-induced PAH. Pathway-based data integration and visualization showed the dysregulated TLR and NLR pathways, including increased expression of TLR2 and NLRP3, and their downstream molecules. Further analysis revealed that the activation of TLR and NLR pathways was associated with up-regulation of damage-associated molecular patterns (DAMPs) and RIPK3-mediated necroptosis was involved in the generation of DAMPs in MCT-induced PAH. Collectively, we identify RIPK3-mediated necroptosis and its triggered TLR and NLR pathways in the progression of pulmonary vascular remodelling, thus providing novel insights into the mechanisms underlying inflammation and immunity in the pathogenesis of PAH.

Indexed as

Signal TransductionAlarminsAnimalsCluster AnalysisGene Expression ProfilingGene Expression RegulationImmunityInflammationModels, BiologicalMonocrotalineNecroptosisNLR ProteinsPulmonary Arterial HypertensionRats, Sprague-DawleyToll-Like ReceptorsTranscriptomeAlarminsMonocrotalineNLR ProteinsToll-Like Receptorsinflammation and immunitynecroptosisNod-like receptorpulmonary arterial hypertensionpulmonary vascular remodellingRNA sequencingToll-like receptor

Identifiers

PMID32860486
PMCPMC7576255
OpenAlexW3082565619

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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.