Evidence map›Paper›PMID 32844595›Full record

ArticleJournal of cellular and molecular medicine2020

Differentially expressed lnc-NOS2P3-miR-939-5p axis in chronic heart failure inhibits myocardial and endothelial cells apoptosis via iNOS/TNFα pathway.

Cuncun Chen, Ming Zong, Ying Lu, Yide Guo, Honggen Lv, Lihong Xie, Zhiyan Fu, Yu Cheng, Yuying Si, Bei Ye and 1 more

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 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Review
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  8. MicroRNA-939 amplifiesFrontiers in immunology · 2024
    Article
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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

11 authors at 1 institution in 1 country.

Cuncun ChenDepartment of Clinical Laboratory, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.ORCID 0000-0001-9473-7289
Ming ZongDepartment of Clinical Laboratory, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Ying LuDepartment of Clinical Laboratory, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Yide GuoDepartment of Clinical Laboratory, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Honggen LvDepartment of Clinical Laboratory, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Lihong XieDepartment of Clinical Laboratory, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Zhiyan FuDepartment of Clinical Laboratory, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Yu ChengDepartment of Clinical Laboratory, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Yuying SiDepartment of Clinical Laboratory, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Bei YeDepartment of Clinical Laboratory, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Lieying FanDepartment of Clinical Laboratory, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Shanghai East Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory cytokine-induced cell apoptosis is important for initiation and progression of chronic heart failure (CHF). Non-coding RNAs, including long non-coding RNAs and microRNAs, have emerged as critical regulators of this pathological process. The role in regulating inflammation and induction to cell apoptosis in CHF is not well understood. This study found CHF patients had elevated serum miR-939-5p, with greater increase in New York Heart Association (NYHA) I-II patients than in NYHA III-IV. Moreover, miR-939-5p was positively correlated with B-type natriuretic peptide (BNP) in NYHA III-IV patients, while not in NYHA I-II. Further study showed miR-939-5p mimics promoted cell proliferation and inhibited inflammatory cytokine-induced apoptosis of HUVECs and H9C2, while inhibition of endogenous miR-939-5p produced the opposite effects. Induced nitric oxide synthase (iNOS) and tumour necrosis factor α (TNFα) were identified as target genes of miR-939-5p. Additionally, lncRNA-NOS2P3 acted as an endogenous sponge RNA to inhibit miR-939-5p expression, regulate the expression of iNOS/TNFα and control inflammation-induced cells apoptosis. These suggest that CHF patients exhibited elevated serum miR-939-5p level especially in NYHA I-II grades. And lnc-NOS2P3-miR-939-5p-iNOS/TNFα pathway regulated inflammatory cytokine-induced endothelial and myocardial cells apoptosis and provided a promising strategy for diagnosis and treatment of CHF.

Indexed as

ApoptosisGene Expression RegulationSignal TransductionBase SequenceChronic DiseaseCytokinesHeart FailureHumansHuman Umbilical Vein Endothelial CellsInflammationMicroRNAsMyocardiumNitric Oxide Synthase Type IIRNA, Long NoncodingTumor Necrosis Factor-alphaCytokinesMicroRNAsMIRN939 microRNA, humanNitric Oxide Synthase Type IIRNA, Long NoncodingTumor Necrosis Factor-alphaapoptosischronic heart failureINOSLncRNA-NOS2P3microRNA-939-5pTNFα

Identifiers

PMID32844595
PMCPMC7576245
OpenAlexW3080937848

What OpenQuestion holds

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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.