Evidence map›Paper›PMID 28281187›Full record

ArticleMolecular and cellular biochemistry2017

MiR-145-5p regulates hypoxia-induced inflammatory response and apoptosis in cardiomyocytes by targeting CD40.

Ming Yuan, Liwei Zhang, Fei You, Jingyu Zhou, Yongjiang Ma, Feifei Yang, Ling Tao

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
7.6field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
  2. Review
  3. Observational
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  6. Review
  7. Review
  8. The Role of ncRNAs in Cardiac Infarction and Regeneration.Journal of cardiovascular development and disease · 2023
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. microRNA-145-5p attenuates acute lung injury via targeting ETS2.The Kaohsiung journal of medical sciences · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Article
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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

7 authors at 3 institutions in 1 country.

Ming YuanDepartment of Cardiology, Xijing Hospital, Changle Xi 17, Xi'an, 710032, Shaanxi, People's Republic of China. 1446534236@qq.com.
Liwei ZhangDepartment of Cardiology, the First Affiliated Hospital of General Hospital of PLA, Beijing, 100048, People's Republic of China.
Fei YouDepartment of Cardiology, Xi'an Central Hospital, Xi'an, 710004, Shaanxi, People's Republic of China.
Jingyu ZhouDepartment of Cardiology, Xijing Hospital, Changle Xi 17, Xi'an, 710032, Shaanxi, People's Republic of China.
Yongjiang MaDepartment of Cardiology, the First Affiliated Hospital of General Hospital of PLA, Beijing, 100048, People's Republic of China.
Feifei YangDepartment of Cardiology, the First Affiliated Hospital of General Hospital of PLA, Beijing, 100048, People's Republic of China.
Ling TaoDepartment of Cardiology, Xijing Hospital, Changle Xi 17, Xi'an, 710032, Shaanxi, People's Republic of China.
First Affiliated Hospital of Chinese PLA General Hospital · CNXijing Hospital · CNXian Central Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

An increasing body of evidence indicates that inflammation and apoptosis are involved in the development of acute myocardial infarction (AMI). In this study, we sought to investigate the specific role and the underlying regulatory mechanism of miR-145-5p in myocardial ischemic injury. H9c2 cardiac cells were exposed to hypoxia to establish a model of myocardial hypoxic/ischemic injury. We found that miR-145-5p was notably down-regulated, while CD40 expression was highly elevated in H9c2 cells following exposure to acute hypoxia. Additionally, hypoxia markedly enhanced the inflammatory response, as reflected by an increase in the secretion of the cytokines IL-1β, TNF-α, and IL-6, whereas the introduction of miR-145-5p effectively suppressed inflammatory factor production triggered by hypoxia. Furthermore, we observed hypoxia stimulation significantly augmented apoptosis accompanied by a decrease in the expression of Bcl-2 and an increase in the expression of Bax, Caspase-3, and Caspase-9. However, augmentation of miR-145-5p led to a dramatic prevention of hypoxia-induced apoptosis. Importantly, we identified CD40 as a direct target of miR-145-5p. Interestingly, the depletion of CD40 with small interfering RNAs (siRNAs) apparently repressed the production of inflammatory cytokines and apoptosis in the setting of acute hypoxic treated. Taken together, these data demonstrated that miR-145-5p may function as a cardiac-protective molecule in myocardial ischemic injury by ameliorating inflammation and apoptosis via negative regulation of CD40. The study gives evidence that miR-145-5p provides an interesting strategy for protecting cardiomyocytes from hypoxia-induced inflammatory response and apoptosis.

Indexed as

ApoptosisApoptosis Regulatory ProteinsCD40 AntigensCell HypoxiaCell LineCytokinesHumansInflammationMicroRNAsMyocardial InfarctionMyocytes, CardiacApoptosis Regulatory ProteinsCD40 AntigensCytokinesMicroRNAsMIRN145 microRNA, humanAcute myocardial infarction (AMI)ApoptosisCD40Inflammatory responseMiR-145-5p

Identifiers

PMID28281187
OpenAlexW2593946321

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.