Evidence map›Paper›PMID 33845782›Full record

ArticleBMC cardiovascular disorders2021

MicroRNA-200b-3p promotes endothelial cell apoptosis by targeting HDAC4 in atherosclerosis.

Fan Zhang, Naixuan Cheng, Jie Du, Haibo Zhang, Congcong Zhang

Open access · goldAbstract readComparative Study
In one paragraph

Article in BMC cardiovascular disorders, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
7.5field-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

33 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025
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  9. Cardioprotective mechanism of Qixuan Yijianing formula in Graves' disease mice using miRNA sequencing approach.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. MicroRNAs Regulate Function in Atherosclerosis and Clinical Implications.Oxidative medicine and cellular longevity · 2023
    Review
  20. Review
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

5 authors at 3 institutions in 1 country.

Fan ZhangBeijing Anzhen Hospital, Capital Medical University, Beijing, China.
Naixuan ChengBeijing Anzhen Hospital, Capital Medical University, Beijing, China.
Jie DuBeijing Anzhen Hospital, Capital Medical University, Beijing, China.
Haibo ZhangBeijing Anzhen Hospital, Capital Medical University, Beijing, China. zhanghb2318@163.com.
Congcong ZhangBeijing Anzhen Hospital, Capital Medical University, Beijing, China. zcc_anzhen@163.com.
Beijing Anzhen Hospital · CNCapital Medical University · CNMinistry of Education of the People's Republic of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEpicardial adipose tissue (EAT) shares the same microcirculation with coronary arteries through coronary arteries branches, and contributes to the development of atherosclerosis. MicroRNAs (miRNAs) are involved in the formation of atherosclerosis. However, the alteration of miRNA profile in EAT during atherosclerosis is still uncovered.

methodsThe miRNA expression profiles of EAT from non-coronary atherosclerosis disease (CON, n = 3) and coronary atherosclerosis disease (CAD, n = 5) patients was performed to detect the differentially expressed miRNA. Then the expression levels of miRNA in other CON (n = 5) and CAD (n = 16) samples were confirmed by realtime-PCR. miR-200b-3p mimic was used to overexpress the miRNA in HUVECs. The apoptosis of HUVECs cells was induced by H

results250 miRNAs were differentially expressed in EAT from CAD patients, which were associated with metabolism, extracellular matrix and inflammation process. Among the top 20 up-regulated miRNAs, the expression levels of miR-200 family members (hsa-miR-200b/c-3p, miR-141-3p and miR-429), which were rich in endothelial cells, were increased in EAT from CAD patients significantly. Upregulation of miR-200 family members was dependent on the oxidative stress. The overexpression of miR-200b-3p could promote endothelial cells apoptosis under oxidative stress by targeting HDAC4 inhibition.

conclusionsOur study suggests that EAT derived miR-200b-3p promoted oxidative stress induced endothelial cells damage by targeting HDAC4, which may provide a new and promising therapeutic target for AS.

Indexed as

ApoptosisApoptosis Regulatory ProteinsAtherosclerosisCells, CulturedCoronary Artery DiseaseHistone DeacetylasesHumansHuman Umbilical Vein Endothelial CellsHydrogen PeroxideLipoproteins, LDLMicroRNAsOxidative StressRepressor ProteinsSignal TransductionApoptosis Regulatory ProteinsHDAC4 protein, humanHistone DeacetylasesHydrogen PeroxideLipoproteins, LDLMicroRNAsMIRN200 microRNA, humanoxidized low density lipoproteinRepressor ProteinsAtherosclerosisEpicardial adipose tissueMiRNA-200 familyMiRNA profileVascular endothelial cells

Identifiers

PMID33845782
PMCPMC8042726
OpenAlexW3156584080

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.