Evidence map›Paper›PMID 30674440›Full record

ArticleEBioMedicine2019

MiR-652-3p inhibition enhances endothelial repair and reduces atherosclerosis by promoting Cyclin D2 expression.

Rongzhong Huang, Zicheng Hu, Yu Cao, Hongrong Li, Hong Zhang, Wenhua Su, Yu Xu, Liwen Liang, N D Melgiri, Lihong Jiang

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

29 citing papers in PubMed, 50 citations in OpenAlex.

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  15. miRNA-486-5p: signaling targets and role in non-malignant disease.Cellular and molecular life sciences : CMLS · 2022
    Review
  16. Article
  17. Article
  18. Regulatory Non-coding RNAs in Atherosclerosis.Handbook of experimental pharmacology · 2022
    Review
  19. Article
  20. 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

10 authors at 3 institutions in 3 countries.

Rongzhong HuangDepartment of Cardiothoracic Surgery, The First People's Hospital of Yunnan Province, Kunming, Yunnan Province, China.
Zicheng HuDepartment of Neurology, Institute of Surgery Research, Daping Hospital, Third Military Medical University, Chongqing, China.
Yu CaoDepartment of Cardiothoracic Surgery, The First People's Hospital of Yunnan Province, Kunming, Yunnan Province, China.
Hongrong LiDepartment of Cardiothoracic Surgery, The First People's Hospital of Yunnan Province, Kunming, Yunnan Province, China.
Hong ZhangDepartment of Cardiology, The First People's Hospital of Yunnan Province, Kunming, Yunnan Province, China.
Wenhua SuDepartment of Cardiology, The First People's Hospital of Yunnan Province, Kunming, Yunnan Province, China.
Yu XuStatistical Laboratory, Chuangxu Institute of Lifescience, Chongqing, China.
Liwen LiangDepartment of Cardiology, The First People's Hospital of Yunnan Province, Kunming, Yunnan Province, China.
N D MelgiriImpactys Foundation for Biomedical Research, San Diego, CA, USA. Electronic address: nd.melgiri@impactys.com.
Lihong JiangDepartment of Cardiothoracic Surgery, The First People's Hospital of Yunnan Province, Kunming, Yunnan Province, China. Electronic address: Lihong-jiang@hotmail.com.
First People's Hospital of Yunnan Province · CNArmy Medical University · CNFoundation for Biomedical Research · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtherosclerosis is a hyperlipidemia-induced condition affecting the arterial wall that damages healthy endothelial cell (EC) function, leading to enhanced risk of atherothrombotic events. Certain microRNAs regulate EC dysfunction in response to hyperlipidemia and may be suitable therapeutic targets to combat atherosclerosis.

methodsmiRNA expression in human ECs was analyzed under various conditions to identify key microRNAs. High-cholesterol diet (HCD)-fed Mir652

findingsmiR-652-3p, which is upregulated in human and murine atherosclerotic plaques, suppresses expression of the endothelial repair gene Ccnd2, thereby enhancing atherosclerotic lesion formation. Post-denudation recovery of ECs was promoted in Mir652

interpretationmiR-652-3p blockade may be a potential therapeutic strategy against atherosclerosis.

Indexed as

Gene Expression Regulation3' Untranslated RegionsAnimalsAntagomirsAtherosclerosisCell LineCyclin D2Disease Models, AnimalEndothelial CellsEndothelium, VascularGene Knockdown TechniquesHumansLipid MetabolismLipoproteins, LDLMiceMicroRNAs3' Untranslated RegionsAntagomirsCyclin D2Lipoproteins, LDLMicroRNAsMIRN652 microRNA, mouseoxidized low density lipoproteinAtherosclerosisCCND2Cyclin D2EndotheliummiR-652

Identifiers

PMID30674440
PMCPMC6413686
OpenAlexW2908620514

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.