Evidence map›Paper›PMID 31994603›Full record

ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2020

miR-26a-5p protects against myocardial ischemia/reperfusion injury by regulating the PTEN/PI3K/AKT signaling pathway.

Xiaowei Xing, Shuang Guo, Guanghao Zhang, Yusheng Liu, Shaojie Bi, Xin Wang, Qinghua Lu

Erratum issuedAbstract read
In one paragraph

Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

56 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  7. Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025
    Review
  8. MicroRNA-100-5p Exacerbates Myocardial Ischemia-Reperfusion Injury Through Downregulation of PRMT5.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Xiaowei XingDepartment of Cardiology, The Second Hospital of Shandong University, Jinan, Shandong, China.ORCID http://orcid.org/0000-0001-6433-2942
Shuang GuoDepartment of Gastroenterology, The Second Hospital of Shandong University, Jinan, Shandong, China.ORCID http://orcid.org/0000-0003-2705-057X
Guanghao ZhangDepartment of Cardiology, The Second Hospital of Shandong University, Jinan, Shandong, China.ORCID http://orcid.org/0000-0002-3298-3211
Yusheng LiuDepartment of Cardiology, The Second Hospital of Shandong University, Jinan, Shandong, China.ORCID http://orcid.org/0000-0003-2317-6546
Shaojie BiDepartment of Cardiology, The Second Hospital of Shandong University, Jinan, Shandong, China.ORCID http://orcid.org/0000-0002-9182-9855
Xin WangDepartment of Cardiology, The Second Hospital of Shandong University, Jinan, Shandong, China.ORCID http://orcid.org/0000-0003-1122-5515
Qinghua LuDepartment of Cardiology, The Second Hospital of Shandong University, Jinan, Shandong, China.ORCID http://orcid.org/0000-0002-4450-3895

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Reperfusion strategies in acute myocardial infarction (AMI) can cause a series of additional clinical damage, defined as myocardial ischemia/reperfusion (I/R) injury, and thus there is a need for effective therapeutic methods to attenuate I/R injury. miR-26a-5p has been proven to be an essential regulator for biological processes in different cell types. Nevertheless, the role of miR-26a-5p in myocardial I/R injury has not yet been reported. We established an I/R injury model in vitro and in vivo. In vitro, we used cardiomyocytes to simulate I/R injury using hypoxia/reoxygenation (H/R) assay. In vivo, we used C57BL/6 mice to construct I/R injury model. The infarct area was examined by TTC staining. The level of miR-26a-5p and PTEN was determined by bioinformatics methods, qRT-PCR, and western blot. In addition, the viability and apoptosis of cardiomyocytes were separately detected by MTT and flow cytometry. The targeting relationship between miR-26a-5p and PTEN was analyzed by the TargetScan website and luciferase reporter assay. I/R and H/R treatment induced myocardial tissue injury and cardiomyocyte apoptosis, respectively. The results showed that miR-26a-5p was down-regulated in myocardial I/R injury. PTEN was found to be a direct target of miR-26a-5p. Furthermore, miR-26a-5p effectively improved viability and inhibited apoptosis in cardiomyocytes upon I/R injury by inhibiting PTEN expression to activate the PI3K/AKT signaling pathway. miR-26a-5p could protect cardiomyocytes against I/R injury by regulating the PTEN/PI3K/AKT pathway, which offers a potential approach for myocardial I/R injury treatment.

Indexed as

AnimalsBlotting, WesternDisease Models, AnimalFlow CytometryMiceMice, Inbred C57BLMicroRNAsMyocardial IschemiaMyocardial Reperfusion InjuryMyocytes, CardiacPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseReal-Time Polymerase Chain ReactionSignal TransductionMicroRNAsMIRN26 microRNA, ratPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktPTEN PhosphohydrolasePTEN protein, human

Identifiers

PMID31994603
PMCPMC6984371

What OpenQuestion 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 OpenQuestion graph.