Evidence map›Paper›PMID 30009269›Full record

ArticleHeliyon2018

Overexpression of miR-221 in sudden death with cardiac hypertrophy patients.

Yu Kakimoto, Masayuki Tanaka, Hideki Hayashi, Keiko Yokoyama, Motoki Osawa

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Heliyon, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.1field-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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
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  10. LncRNA TUG1 contributes to cardiac hypertrophy via regulating miR-29b-3p.In vitro cellular & developmental biology. Animal · 2019
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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 1 institution in 1 country.

Yu KakimotoDepartment of Forensic Medicine, Tokai University School of Medicine, Kanagawa, Japan.
Masayuki TanakaSupport Center for Medical Research and Education, Tokai University, Kanagawa, Japan.
Hideki HayashiSupport Center for Medical Research and Education, Tokai University, Kanagawa, Japan.
Keiko YokoyamaSupport Center for Medical Research and Education, Tokai University, Kanagawa, Japan.
Motoki OsawaDepartment of Forensic Medicine, Tokai University School of Medicine, Kanagawa, Japan.
Tokai University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCardiac hypertrophy is a well-known risk factor for heart failure and sudden cardiac death (SCD). On the other hand, physiological cardiac hypertrophy is often observed in young healthy men, and it is difficult to predict SCD in cardiac hypertrophy subjects who do not show symptoms of heart failure. MicroRNAs (miRNAs) widely regulate biological activity and play pivotal roles in heart failure progression. In this study, we investigated whether miRNA expression is altered in SCD with cardiac hypertrophy (SCH).

methodsCardiac tissues were sampled at autopsy from SCH patients, compensated cardiac hypertrophy (CCH) subjects who died of causes other than heart failure, and control cases without cardiac hypertrophy or heart failure. After histopathological examination, we performed deep sequencing and quantitative PCR of cardiac miRNAs. RESULTS AND DISCUSSION: Although SCH and CCH showed indistinguishable histological features, their miRNA expression signatures were distinct. Among the 240 miRNAs stably detected in the heart, 8 were differentially expressed between SCH and CCH. Specifically, miR-221 increased in SCH compared to CCH and control cases. The significant elevation of cardiac miR-221 in SCH patients is correlated with lethal outcomes. Thus, our results indicate that an elevated miR-221 level is potentially associated with an increased risk of SCD in subjects with cardiac hypertrophy.

Indexed as

CardiologyClinical geneticsMedicinePathology

Identifiers

PMID30009269
PMCPMC6041564
OpenAlexW2806335221

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.