Evidence map›Paper›PMID 28025989›Full record

ArticleInternational journal of molecular medicine2016

MicroRNA-142-3p inhibits hypoxia/reoxygenation‑induced apoptosis and fibrosis of cardiomyocytes by targeting high mobility group box 1.

Yi Wang, Min Ouyang, Qiong Wang, Zaijin Jian

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

Article in International journal of molecular medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed, 2 pooled it
4.8field-weighted citation impact, top 4% 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

55 citing papers in PubMed, 2 syntheses or guidelines pooled it, 85 citations in OpenAlex.

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  14. MicroRNAs regulating signaling pathways in cardiac fibrosis: potential role of the exercise training.American journal of physiology. Heart and circulatory physiology · 2024
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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

4 authors at 2 institutions in 1 country.

Yi WangGeriatric Department, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.
Min OuyangGeriatric Department, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.
Qiong WangGeriatric Department, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.
Zaijin JianGeriatric Department, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, P.R. China.
Central South University · CNSecond Xiangya Hospital of Central South University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial ischemia/reperfusion (I/R) injury may cause the apoptosis of cardiomyocytes as well as cardiac fibrosis, which is characterized as the transdifferentiation of fibroblasts to myofibroblasts and collagen deposition. MicroRNAs (miRNAs or miRs) have been demonstrated to be involved in myocardial I/R injury. However, the underlying molecular mechanism remains largely unclear. In the present study, mouse cardiomyocyte M6200 cells were treated with hypoxia/reoxygenation (H/R). Our data indicated that H/R treatment led to cell apoptosis, the increased expression of fibrosis‑related proteins, namely collagen I, II, III, and fibronectin, as well as the downregulation of miR-142-3p in M6200 cells. Overexpression of miR-142-3p suppressed the H/R-induced apoptosis and fibrosis of M6200 cells. Bioinformatics analysis and a Dual‑Luciferase reporter assay further identified high mobility group box 1 (HMGB1) as a direct target gene of miR-142-3p, and miR-142-3p negatively regulated the protein level of HMGB1 in M6200 cells. Furthermore, knockdown of HMGB1 enhanced cell proliferation whereas it inhibited the apoptosis and fibrosis of M6200 cells. In addition, TGF-β1/Smad3 signaling was suggested to be involved in the miR-142-3p/HMGB1-mediated apoptosis and fibrosis of M6200 cells treated with H/R. Taken together, the findings of the present study demonstrate that miR-142-3p inhibits H/R-induced apoptosis and fibrosis of cardiomyocytes, partly at least, by the direct inhibition of HMGB1 expression. Therefore, these findings have increased our understanding of the pathogenesis of H/R-induced myocardial injury.

Indexed as

AnimalsApoptosisBase SequenceBlotting, WesternCell HypoxiaCell LineFibrosisFlow CytometryGene Knockdown TechniquesHMGB1 ProteinMiceMicroRNAsMyocytes, CardiacOxygenPhosphorylationReal-Time Polymerase Chain ReactionHMGB1 ProteinMicroRNAsMirn142 microRNA, mouseOxygenRNA, MessengerSmad3 ProteinTransforming Growth Factor beta1

Identifiers

PMID28025989
PMCPMC5065300
OpenAlexW2524258931

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.