Evidence map›Paper›PMID 31432137›Full record

ArticleMolecular medicine reports2019

MicroRNA‑217 is involved in the progression of atherosclerosis through regulating inflammatory responses by targeting sirtuin 1.

Liyun Zhang, Juan Chen, Qin He, Ze Chao, Xuyong Li, Manhua Chen

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Epigenetic Mechanisms in Heart Diseases.Reviews in cardiovascular medicine · 2025
    Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. The sirtuin family in health and disease.Signal transduction and targeted therapy · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
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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

6 authors at 1 institution in 1 country.

Liyun ZhangDepartment of Cardiology, Wuhan Central Hospital, Wuhan, Hubei 430015, P.R. China.
Juan ChenDepartment of Cardiology, Wuhan Central Hospital, Wuhan, Hubei 430015, P.R. China.
Qin HeDepartment of Cardiology, Wuhan Central Hospital, Wuhan, Hubei 430015, P.R. China.
Ze ChaoDepartment of Cardiology, Wuhan Central Hospital, Wuhan, Hubei 430015, P.R. China.
Xuyong LiDepartment of Cardiology, Wuhan Central Hospital, Wuhan, Hubei 430015, P.R. China.
Manhua ChenDepartment of Cardiology, Wuhan Central Hospital, Wuhan, Hubei 430015, P.R. China.
Central Hospital of Wuhan · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is a chronic inflammatory disease, and it is a global clinical problem. The development of new and effective therapeutic targets for atherosclerosis is necessary. A number of microRNAs (miRNAs) have been demonstrated to serve a crucial role in atherosclerosis. However, the role of miRNA (miR)‑217 in atherosclerosis remains unclear. Therefore, the aim of the present study was to investigate the role and mechanism of miR‑217 in atherosclerosis. The level of miR‑217 was detected in the blood of patients with atherosclerosis using reverse transcription‑quantitative PCR. THP‑1 acute monocytic leukemia cells were treated with oxidized low‑density lipoprotein (ox‑LDL) to develop an atherosclerotic cell model of macrophages. The relationship between miR‑217 and sirtuin 1 (SIRT1) was determined by TargetScan and dual luciferase reporter assay. Cell apoptosis was measured by flow cytometry. Production of pro‑inflammatory factors and triglyceride (TG) and total cholesterol (TC) levels were also determined. The results demonstrated that miR‑217 was significantly upregulated in atherosclerosis. SIRT1 was demonstrated to be a direct target of miR‑217 and was downregulated in atherosclerosis. Downregulation of miR‑217 significantly inhibited ox‑LDL‑induced TG and TC level increase, cell apoptosis and the upregulation of the pro‑inflammatory factors tumor necrosis factor α, interleukin (IL)‑6 and IL‑1β. Additionally, the SIRT1/AMP‑activated protein kinase α/NF‑κB pathway was at least partially involved in modulating the effects of miR‑217 inhibition on THP‑1 cells treated with ox‑LDL. In addition, the effects of miR‑217 downregulation on ox‑LDL‑treated THP‑1 cells were eliminated by SIRT1 silencing. In conclusion, the results of the present study indicated that miR‑217 downregulation may relieve atherosclerosis through the inhibition of macrophage apoptosis and inflammatory response by targeting SIRT1.

Indexed as

ApoptosisAgedAtherosclerosisCytokinesDisease ProgressionFemaleHumansInflammationMacrophagesMaleMicroRNAsMiddle AgedSirtuin 1THP-1 CellsCytokinesMicroRNAsMIRN217 microRNA, humanSIRT1 protein, humanSirtuin 1

Identifiers

PMID31432137
PMCPMC6755250
OpenAlexW2967035089

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.