Evidence map›Paper›PMID 27175593›Full record

ArticleOncotarget2016

Down-regulation of microRNA-320 suppresses cardiomyocyte apoptosis and protects against myocardial ischemia and reperfusion injury by targeting IGF-1.

Chun-Li Song, Bin Liu, Hong-Ying Diao, Yong-Feng Shi, Ji-Chang Zhang, Yang-Xue Li, Ning Liu, Yun-Peng Yu, Guan Wang, Jin-Peng Wang and 1 more

RetractedOpen access · diamondAbstract readRetracted Publication
PubMed Full text at PMC Publisher
In one paragraph

Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
4.2field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 1 institution in 1 country.

Chun-Li SongDepartment of Cardiology, The Second Hospital of Jilin University, Changchun 130041, P. R. China.
Bin LiuDepartment of Cardiology, The Second Hospital of Jilin University, Changchun 130041, P. R. China.
Hong-Ying DiaoDepartment of Cardiology, The Second Hospital of Jilin University, Changchun 130041, P. R. China.
Yong-Feng ShiDepartment of Cardiology, The Second Hospital of Jilin University, Changchun 130041, P. R. China.
Ji-Chang ZhangDepartment of Cardiology, The Second Hospital of Jilin University, Changchun 130041, P. R. China.
Yang-Xue LiDepartment of Cardiology, The Second Hospital of Jilin University, Changchun 130041, P. R. China.
Ning LiuDepartment of Cardiology, The Second Hospital of Jilin University, Changchun 130041, P. R. China.
Yun-Peng YuDepartment of Cardiology, The Second Hospital of Jilin University, Changchun 130041, P. R. China.
Guan WangDepartment of Cardiology, The Second Hospital of Jilin University, Changchun 130041, P. R. China.
Jin-Peng WangDepartment of Cardiology, The Second Hospital of Jilin University, Changchun 130041, P. R. China.
Qian LiDepartment of Cardiology, The Second Hospital of Jilin University, Changchun 130041, P. R. China.
Second Affiliated Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Insulin-like growth factor-1 (IGF-1) is an important regulator of cardiomyocyte homeostasis and cardiac structure, and the prosurvival and antiapoptotic effects of IGF-1 have been investigated. However, the effect of microRNA-320 (miR-320) in ischemia and reperfusion (I/R) by targeting IGF-1 is rarely discussed. We investigated the role of miR-320 in I/R injury. A total of 192 healthy female Wistar rats were divided into eight groups (n = 24). Rat heart I/R model was established. Hemodynamics, infarct size weight (ISW), heart function, and rat cardiomyocyte apoptosis were measured. Hypoxia-reoxygenation (H/R) in rat cardiomyocyte was used to simulate the I/R process. The mRNA levels of miR-320 and IGF-1, and proteins levels of IGF-1, IGF-1R, p-IGF-1R, p-ASK1, p-JNK, p-p38, Bcl-2, Bax and Caspase-3 were measured. In vivo inhibition of miR-320 expression significantly increased IGF-1 and IGF-1R mRNA levels, elevated the absolute values of SBP, DBP, MAP, ± dp/dtmax, LVEF and LVFS, decreased ISW, LVESD and LVEDd and the number of TUNEL positive cells, lowered the levels of p-ASK1, p-JNK, p-p38, Bax and Caspase-3 and increased expression of Bcl-2 compared to the I/R + NC group. Compared to H/R + NC group in vitro, miR-320 inhibition increased IGF-1 mRNA levels, inhibited cardiomyocyte apoptosis, down-regulated p-ASK, p-JNK, p-p38, Bax and Caspase-3 levels, and up-regulated Bcl-2 level. MiR-320 inhibition target elevated IGF-1 mRNA and protein levels, suppress early cardiomyocyte apoptosis of I/R, and inhibited ASK1-JNK/p38 pathway, which provides a new target for clinical study of I/R injury.

Indexed as

Down-RegulationAnimalsApoptosisBinding SitesCaspase 3FemaleHemodynamicsInsulin-Like Growth Factor IMicroRNAsMyocardial InfarctionMyocardial IschemiaMyocardiumMyocytes, CardiacProto-Oncogene Proteins c-bcl-2RatsRats, WistarCaspase 3Insulin-Like Growth Factor IMicroRNAsMIRN320 microRNA, ratProto-Oncogene Proteins c-bcl-2apoptosis ratecardiomyocyteshypoxia-reoxygenationischemia-reperfusionmicroRNA-320

Identifiers

PMID27175593
PMCPMC5129967
OpenAlexW2379128117

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.