Evidence map›Paper›PMID 31178952›Full record

ArticleOxidative medicine and cellular longevity2019

miR-181c-5p Exacerbates Hypoxia/Reoxygenation-Induced Cardiomyocyte Apoptosis via Targeting PTPN4.

Liang Ge, Yin Cai, Fan Ying, Hao Liu, Dengwen Zhang, Yanjing He, Lei Pang, Dan Yan, Aimin Xu, Haichun Ma and 1 more

Open access · hybridAbstract read
In one paragraph

Article in Oxidative medicine and cellular longevity, 2019. 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
3.3field-weighted citation impact, top 7% 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, 58 citations in OpenAlex.

  1. Article
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  7. MicroRNA-181 in cardiovascular disease: Emerging biomarkers and therapeutic targets.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Review
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  16. MicroRNA-181c-5p modulates phagocytosis efficiency in bone marrow-derived macrophages.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    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 4 institutions in 2 countries.

Liang GeDepartment of Anesthesiology, The First Hospital, Jilin University, Jilin, China.
Yin CaiState Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Hong Kong.
Fan YingState Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Hong Kong.
Hao LiuDepartment of Anesthesiology, The University of Hong Kong, Hong Kong.
Dengwen ZhangDepartment of Anesthesiology, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China.
Yanjing HeState Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Hong Kong.
Lei PangDepartment of Anesthesiology, The First Hospital, Jilin University, Jilin, China.ORCID 0000-0002-2285-2728
Dan YanState Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Hong Kong.
Aimin XuState Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Hong Kong.
Haichun MaDepartment of Anesthesiology, The First Hospital, Jilin University, Jilin, China.ORCID 0000-0002-8467-5421
Zhengyuan XiaState Key Laboratory of Pharmaceutical Biotechnology, The University of Hong Kong, Hong Kong.ORCID 0000-0002-7002-5524
University of Hong Kong · HKJilin University · CNGuangdong Academy of Medical Sciences · CNSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundActivation of cell apoptosis is a major form of cell death during myocardial ischemia/reperfusion injury (I/RI). Therefore, examining ways to control cell apoptosis has important clinical significance for improving postischemic recovery. Clinical evidence demonstrated that miR-181c-5p was significantly upregulated in the early phase of myocardial infarction. However, whether or not miR-181c-5p mediates cardiac I/RI through cell apoptosis pathway is unknown. Thus, the present study is aimed at investigating the role and the possible mechanism of miR-181c-5p in apoptosis during I/R injury by using H9C2 cardiomyocytes. METHODS AND

resultsThe rat origin H9C2 cardiomyocytes were subjected to hypoxia/reoxygenation (H/R, 6 hours hypoxia followed by 6 hours reoxygenation) to induce cell injury. The results showed that H/R significantly increased the expression of miR-181c-5p but not miR-181c-3p in H9C2 cells. In line with this, in an

conclusionsThese findings suggested that miR-181c-5p exacerbates H/R-induced cardiomyocyte injury and apoptosis

Indexed as

AnimalsApoptosisCell HypoxiaMaleMicroRNAsMyocardial Reperfusion InjuryMyocytes, CardiacProtein Tyrosine Phosphatase, Non-Receptor Type 4RatsRats, Sprague-DawleyTransfectionMicroRNAsMIRN181 microRNA, ratProtein Tyrosine Phosphatase, Non-Receptor Type 4Ptpn4 protein, rat

Identifiers

PMID31178952
PMCPMC6501226
OpenAlexW2939004866

What Socratic 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 Socratic graph.