Evidence map›Paper›PMID 33352533›Full record

ArticleAging2020

Inhibition of Exo-miR-19a-3p derived from cardiomyocytes promotes angiogenesis and improves heart function in mice with myocardial infarction via targeting HIF-1α.

Lianping Gou, Cheng Xue, Xiaoyan Tang, Zhiyuan Fang

Open access · greenAbstract read
In one paragraph

Article in Aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 12% 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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

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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.

Lianping GouDepartment of Cardiovascular Medicine, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan Province, China.
Cheng XueDepartment of Cardiovascular Medicine, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan Province, China.
Xiaoyan TangDepartment of General Practitioner, Affiliated Hospital of North Sichuan Medical College, Nanchong, Sichuan Province, China.
Zhiyuan FangDepartment of Medicine, Shanxi Provincial People’s Hospital, Xi'an, Shanxi Province, China.
Affiliated Hospital of North Sichuan Medical College · CNShaanxi Provincial People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMyocardial infarction (MI), a common presentation for cardiovascular disease, is caused by reduction of blood flow and oxygen supply and is one of the main causes of death worldwide. MicroRNAs participate in multiple physiological and pathological processed and play crucial role in myocardial infarction.

resultsqRT-PCR analysis showed that expression level of miR-19a-3p was increased in serum of patient with MI.

conclusionsIn conclusion, our finding indicated that miR-19a-3p inhibited endothelial cells proliferation and angiogenesis via targeting HIF-1α and attenuated heart function of mice after MI, and suggested a new mechanism of cell-to-cell communication between cardiomyocytes and endothelial cells.

Indexed as

Neovascularization, PhysiologicAnimalsAntagomirsCase-Control StudiesCell ProliferationCells, CulturedDisease Models, AnimalEndothelial CellsExosomesGene Expression RegulationHumansHypoxia-Inducible Factor 1, alpha SubunitMaleMice, Inbred C57BLMicroRNAsMyocardial InfarctionAntagomirsHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitMicroRNAsMIRN19A microRNA, humanMIRN19a microRNA, mouseangiogenesisexosomeHIF-1αmiR-19a-3pmyocardial infarction

Identifiers

PMID33352533
PMCPMC7762502
OpenAlexW3049074885

What OpenQuestion holds

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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.