Evidence map›Paper›PMID 32291604›Full record

ArticleJournal of bioenergetics and biomembranes2020

MiR-703 protects against hypoxia/reoxygenation-induced cardiomyocyte injury via inhibiting the NLRP3/caspase-1-mediated pyroptosis.

Xiaoliang Wei, Hu Peng, Ming Deng, Zongming Feng, Changnong Peng, Dahao Yang

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of bioenergetics and biomembranes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Programmed cardiomyocyte death in myocardial infarction.Apoptosis : an international journal on programmed cell death · 2025
    Review
  6. Signaling pathways and targeted therapy for myocardial infarction.Signal transduction and targeted therapy · 2022
    Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. NormothermicFrontiers in cell and developmental biology · 2021
    Article
  12. Frontiers in cellular and infection microbiology · 2021
    Article
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

6 authors at 3 institutions in 1 country.

Xiaoliang WeiThe Center of Cardiovascular Diseases, the Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, 519000, China.
Hu PengThe Center of Cardiovascular Diseases, the Fifth Affiliated Hospital of Sun Yat-Sen University, Zhuhai, 519000, China.
Ming DengDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen Sun Yat-sen Cardiovascular Hospital, Shenzhen, 518057, China.
Zongming FengDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen Sun Yat-sen Cardiovascular Hospital, Shenzhen, 518057, China.
Changnong PengDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen Sun Yat-sen Cardiovascular Hospital, Shenzhen, 518057, China. Pengchangnong1965@163.com.
Dahao YangDepartment of Cardiology, Fuwai Hospital, Chinese Academy of Medical Sciences, Shenzhen Sun Yat-sen Cardiovascular Hospital, Shenzhen, 518057, China. yangdahao@126.com.
Chinese Academy of Medical Sciences & Peking Union Medical College · CNFifth Affiliated Hospital of Sun Yat-sen University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial infarction represents one of the severe cardiovascular diseases and is one of the high-risk factors for mortality, and ischemia/reperfusion (I/R) injury is one of the risk factors that contribute to the high mortality of myocardial infarction. MicroRNAs have been proven as key regulators in various diseases including myocardial infarction. The present study was sought to determine the role of miR-703 in the myocardial I/R injury and to explore detailed mechanisms. Hypoxia/reoxygenation (H/R) treatment repressed cell viability, increased cytotoxicity and pyroptosis in mouse cardiomyocytes. More importantly, we found that miR-703 was suppressed in mouse cardiomyocytes upon H/R stimulation. Restoration of miR-703 expression in mouse cardiomyocytes counteracted the H/R-induced cytotoxicity and pyroptosis in mouse cardiomyocytes; and the effects of miR-703 inhibition on cell viability and pyroptosis were similar to that of H/R treatment in mouse cardiomyocytes. In a further investigation, we found that NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) was targeted and repressed by miR-703 in mouse cardiomyocytes. NLRP3 knockdown also attenuated H/R-induced cytotoxicity and pyroptosis in mouse cardiomyocytes. In the mechanistic perspective, NLRP3 enforced expression disrupted the protective effects of miR-703 restoration on the H/R-induced cytotoxicity and pyroptosis in mouse cardiomyocytes. Our results for the first time demonstrate the protective actions of miR-703 in the H/R-induced mouse cardiomyocyte injury. More importantly, miR-703 protects against H/R-induced cardiomyocyte injury via inhibiting the NLRP3/caspase-1-mediated pyroptosis.

Indexed as

AnimalsCaspase 1Cell HypoxiaMiceMicroRNAsMyocytes, CardiacNLR Family, Pyrin Domain-Containing 3 ProteinPyroptosisTransfectionCaspase 1MicroRNAsNLR Family, Pyrin Domain-Containing 3 ProteinHypoxia/reoxygenationIschemia/reperfusionmiR-703Mouse cardiomyocytesNLRP3Pyroptosis

Identifiers

PMID32291604
OpenAlexW3015849054

What OpenQuestion holds

Textmetadata
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.