Evidence map›Paper›PMID 30906453›Full record

ArticleExperimental and therapeutic medicine2019

Decoy receptor-3 regulates inflammation and apoptosis via PI3K/AKT signaling pathway in coronary heart disease.

Xinjing Chen, Rehua Wang, Wei Chen, Li Lai, Zhiliang Li

Open access · diamondAbstract read
In one paragraph

Article in Experimental and therapeutic medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Research Progress of DcR3 in the Diagnosis and Treatment of Sepsis.International journal of molecular sciences · 2023
    Review
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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

5 authors at 4 institutions in 1 country.

Xinjing ChenDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
Rehua WangDepartment of Cardiology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou, Fujian 350001, P.R. China.
Wei ChenDepartment of Cardiology, Fujian Provincial Hospital, Fujian Medical University, Fuzhou, Fujian 350001, P.R. China.
Li LaiFujian Key Laboratory of Cardiovascular Disease, Fujian Provincial Hospital, Fujian Medical University, Fuzhou, Fujian 350001, P.R. China.
Zhiliang LiDepartment of Cardiology, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, P.R. China.
Fujian Medical University · CNFujian Provincial Hospital · CNSouthern Medical University · CNZhujiang Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronary heart disease is a disease characterized by coronary artery atherosclerosis lesions caused by vascular cavity stenosis, occlusion, myocardial ischemia, hypoxia or necrosis. Previous studies have demonstrated that decoy receptor-3 (DCR-3) can act as a pleiotropic immunomodulation for enhancing angiogenesis, which may be associated with the progression of coronary heart disease. In the present study, ELISA assay was used to investigate the plasma concentration level of DCR-3 in patients with coronary heart disease. The mRNA and protein level of DCR-3 in myocardial cells were determined by reverse transcription-quantitative polymerase chain reaction and western blotting, respectively. The role and molecular mechanism of DCR-3 was also evaluated in myocardial cells in mice with coronary heart disease. The role of small interfering RNA that targeted phosphoinositide 3-kinase (PI3K) in DCR-3 mediated apoptosis was confirmed by terminal deoxynucleotidyl-transferase-mediated dUTP nick end labeling and immunofluorescence. C57BL/6 mice with coronary heart disease were used to evaluate the efficacy of DCR-3 on inflammation and apoptosis. The data indicated that plasma concentration level of DCR-3 was downregulated in mice with coronary heart disease and that DCR-3 administration improved symptoms of coronary heart disease and prolonged survival of mice with coronary heart disease. In addition, it was demonstrated that DCR-3 treatment suppressed the inflammatory response and apoptosis of myocardial cells. Circulating DCR-3 concentration levels may be identified as a predictor of coronary heart disease and prognosis of coronary heart disease. Notably, it was also demonstrated that DCR-3 inhibited inflammatory factor expression levels by regulation of the PI3K/protein kinase B (AKT) signaling pathway. Taken together, these results indicate that increasing circulating DCR-3 plasma concentration is associated with degree of coronary heart disease, suggesting that DCR-3 may be a promising drug for the treatment of coronary heart disease via regulating inflammation and apoptosis through the PI3K/AKT signaling pathway.

Indexed as

apoptosiscoronary heart diseasedecoyreceptor-3inflammation

Identifiers

PMID30906453
PMCPMC6425242
OpenAlexW2914390211

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.