Evidence map›Paper›PMID 35202001›Full record

ArticleAging2022

miR-223-3p inhibits the progression of atherosclerosis via down-regulating the activation of MEK1/ERK1/2 in macrophages.

Daofeng You, Qiuge Qiao, Katsushige Ono, Mei Wei, Wenyun Tan, Cuihua Wang, Yangong Liu, Gang Liu, Mingqi Zheng

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 12% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

  1. Pooled it
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  5. Connecting the Dots: How MicroRNAs Link Asthma and Atherosclerosis.International journal of molecular sciences · 2025
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  19. The Association of Monocytes/High-Density Lipoprotein Cholesterol Ratio With Cardiovascular-Kidney-Metabolic Syndrome and Its All-Cause Mortality - Evidence From NHANES 2003-2018.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis
    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

9 authors at 3 institutions in 2 countries.

Daofeng YouHebei Medical University First Affiliated Hospital, Shijiazhuang 050023, Hebei, China.
Qiuge QiaoHebei Medical University Second Affiliated Hospital, Shijiazhuang 050023, Hebei, China.
Katsushige OnoDepartment of Pathophysiology, Oita University School of Medicine, Hasama, Yufu, Ōita-shi, Japan.
Mei WeiHebei Medical University First Affiliated Hospital, Shijiazhuang 050023, Hebei, China.
Wenyun TanHebei Medical University First Affiliated Hospital, Shijiazhuang 050023, Hebei, China.
Cuihua WangHebei Medical University First Affiliated Hospital, Shijiazhuang 050023, Hebei, China.
Yangong LiuHebei Medical University First Affiliated Hospital, Shijiazhuang 050023, Hebei, China.
Gang LiuHebei Medical University First Affiliated Hospital, Shijiazhuang 050023, Hebei, China.
Mingqi ZhengHebei Medical University First Affiliated Hospital, Shijiazhuang 050023, Hebei, China.
First Affiliated Hospital of Hebei Medical University · CNHebei Medical University · CNOita University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundmicroRNAs (miRNAs) have drawn more attention to the progression of atherosclerosis (AS), due to their noticeable inflammation function in cardiovascular disease. Macrophages play a crucial role in disrupting atherosclerotic plaque, thereby we explored the involvement of miR-223-3p in the inflammatory response in macrophages.

methodsRT-qPCR was used to analyze the miR-223-3p levels in carotid arteries and serum of AS patients. ROC curve was used to assess the diagnostic value of miR-223-3p. Movat staining was applied to evaluate the morphological differences. FISH was used to identify the expression of miR-223-3p in macrophages of atherosclerotic lesions. Bioinformatic analysis was performed. Double-immunofluorescence and western blot were performed to assess the inflammatory cytokine secretion and p-ERK1/2. C16-PAF was injected into the culture medium of the miR-223-3p mimic/NC-transfected macrophages with ox-LDL.

resultsMiR-223-3p was up-regulated in AS patients and was associated with a higher overall survival rate. MiR-223-3p was co-localized with CD68+ macrophages in vulnerable atherosclerotic lesions. MiR-223-3p mimics decreased atherosclerotic lesions, macrophages numbers whereas increased SMCs numbers in the lesions. The TNF-a immune-positive areas were reduced by miR-223-3p mimics. MAP2K1 was negatively associated with miR-223-3p. MiR-223-3p mimics reduced the inflammation and the MEK1/ERK1/2 signaling pathway

conclusionsMiR-223-3p negatively regulates inflammatory responses by the MEK1/ERK1/2 signaling pathway. Our study provides new insight into how miR-223-3p protects against atherosclerosis, representing a broader therapeutic prospect for treating atherosclerosis by miR-223-3p.

Indexed as

AtherosclerosisMicroRNAsHumansInflammationMacrophagesMAP Kinase Signaling SystemMicroRNAsMIR223, humanatherosclerosisinflammatory responsemacrophagesMEK1/ERK1/2 signaling pathwaymiR-223-3p

Identifiers

PMID35202001
PMCPMC8908932
OpenAlexW4213423774

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.