Evidence map›Paper›PMID 32939968›Full record

ArticleJournal of cellular and molecular medicine2020

HIF-1α-induced up-regulation of microRNA-126 contributes to the effectiveness of exercise training on myocardial angiogenesis in myocardial infarction rats.

Wei Song, Qiaoqin Liang, Mengxin Cai, Zhenjun Tian

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 9% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 62 citations in OpenAlex.

  1. Pooled it
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  7. MicroRNA-126 as an endogenous molecule for hypoxic/ischemic tolerance in neuroprotection.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025
    Review
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  12. miR-126: a bridge between cancer and exercise.Cancer cell international · 2025
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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 1 institution in 1 country.

Wei SongInstitute of Sports and Exercise Biology, Shaanxi Normal University, Xi'an, China.ORCID 0000-0003-0166-2308
Qiaoqin LiangInstitute of Sports and Exercise Biology, Shaanxi Normal University, Xi'an, China.
Mengxin CaiInstitute of Sports and Exercise Biology, Shaanxi Normal University, Xi'an, China.
Zhenjun TianInstitute of Sports and Exercise Biology, Shaanxi Normal University, Xi'an, China.ORCID 0000-0002-8747-6161
Shaanxi Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exercise training (ET) is a non-drug natural rehabilitation approach for myocardial infarction (MI). Among the numerous beneficial effects of ET, myocardial angiogenesis is indispensable. In the present study, we investigated the role and mechanism of HIF-1α and miR-126 in ET-induced MI myocardial angiogenesis which may provide new insights for MI treatment. Rat model of post-MI and human umbilical vein endothelial cells (HUVECs) were employed for our research. Histomorphology, immunohistochemistry, quantitative real-time PCR, Western blotting and small-interfering RNA (siRNA) transfection were applied to evaluate the morphological, functional and molecular mechanisms. In vivo results showed that 4-week ET could significantly increase the expression of HIF-1α and miR-126 and reduce the expression of PIK3R2 and SPRED1, while 2ME2 (HIF-1α inhibitor) partially attenuated the effect of ET treatment. In vitro results showed that HIF-1α could trigger expression of miR-126 in HUVECs in both normoxia and hypoxia, and miR-126 may be involved in the tube formation of HUVECs under hypoxia through the PI3K/AKT/eNOS and MAPK signalling pathway. In conclusion, we revealed that HIF-1α, whose expression experiences up-regulation during ET, could function as an upstream regulator to miR-126, resulting in angiogenesis promotion through the PI3K/AKT/eNOS and MAPK signalling pathway and subsequent improvement of the MI heart function.

Indexed as

Neovascularization, PathologicPhysical Conditioning, AnimalAnimalsCollagenHemodynamicsHumansHuman Umbilical Vein Endothelial CellsHypoxiaHypoxia-Inducible Factor 1, alpha SubunitMaleMicroRNAsMyocardial InfarctionRatsRats, Sprague-DawleyRNA, Small InterferingSignal TransductionCollagenHIF1A protein, humanHif1a protein, ratHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN126 microRNA, humanMIRN126 microRNA, ratRNA, Small Interferingexercise trainingHIF-1αmiR-126myocardial angiogenesismyocardial infarction

Identifiers

PMID32939968
PMCPMC7701575
OpenAlexW3086265525

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.