Evidence map›Paper›PMID 38919016›Full record

ArticleBMB reports2024

miR-328-5p functions as a critical negative regulator in early endothelial inflammation and advanced atherosclerosis.

Yangxia Zhang, Yingke Li, Zhisheng Han, Qingyang Huo, Longkai Ji, Xuejia Liu, Han Li, Xinxing Zhu, Zhipeng Hao

Abstract readNews
PubMed Full text at PMC
In one paragraph

Article in BMB reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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.

Yangxia ZhangHenan Joint International Research Laboratory of Stem Cell Medicine, School of Medical Engineering, Xinxiang Medical University, Xinxiang 453003, China.
Yingke LiHenan Joint International Research Laboratory of Stem Cell Medicine, School of Medical Engineering, Xinxiang Medical University, Xinxiang 453003, China.
Zhisheng HanHenan Joint International Research Laboratory of Stem Cell Medicine, School of Medical Engineering, Xinxiang Medical University, Xinxiang 453003, China.
Qingyang HuoHenan Joint International Research Laboratory of Stem Cell Medicine, School of Medical Engineering, Xinxiang Medical University, Xinxiang 453003, China.
Longkai JiHenan Joint International Research Laboratory of Stem Cell Medicine, School of Medical Engineering, Xinxiang Medical University, Xinxiang 453003, China.
Xuejia LiuStem Cells and Biotherapy Engineering Research Center of Henan, College of Life Science and Technology, Xinxiang Medical University, Xinxiang 453003, China.
Han LiStem Cells and Biotherapy Engineering Research Center of Henan, College of Life Science and Technology, Xinxiang Medical University, Xinxiang 453003, China.
Xinxing ZhuHenan Joint International Research Laboratory of Stem Cell Medicine, School of Medical Engineering, Xinxiang Medical University, Xinxiang 453003; Department of Respiratory and Critical Care Medicine, Anhui Province Key Laboratory of Clinical and Preclinical Research in Respiratory Disease, First Affiliated Hospital, Bengbu Medical University, Bengbu 233004, China.
Zhipeng HaoDepartment of Thoracic Surgery of Tongji Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan 430030, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Early proatherogenic inflammation constitutes a significant risk factor for atherogenesis development. Despite this, the precise molecular mechanisms driving this pathological progression largely remain elusive. Our study unveils a pivotal role for the microRNA miR-328-5p in dampening endothelial inflammation by modulating the stability of JUNB (JunB proto-oncogene). Perturbation of miR-328-5p levels results in heightened monocyte adhesion to endothelial cells and enhanced transendothelial migration, while its overexpression mitigates these inflammatory processes. Furthermore, miR-328-5p hinders macrophage polarization toward the pro-inflammatory M1 phenotype, and exerts a negative influence on atherosclerotic plaque formation in vivo. By pinpointing JUNB as a direct miR-328-5p target, our research underscores the potential of miR-328-5p as a therapeutic target for inflammatory atherosclerosis. Reintroduction of JUNB effectively counteracts the anti-atherosclerotic effects of miR-328-5p, highlighting the promise of pharmacological miR-328-5p targeting in managing inflammatory atherosclerosis. [BMB Reports 2024; 57(8): 375-380].

Indexed as

AtherosclerosisInflammationMicroRNAsProto-Oncogene MasAnimalsCell AdhesionCell MovementEndothelial CellsHumansHuman Umbilical Vein Endothelial CellsMacrophagesMiceMonocytesPlaque, AtheroscleroticMAS1 protein, humanMicroRNAsMIRN328 microRNA, humanProto-Oncogene Mas

Identifiers

PMID38919016
PMCPMC11362139

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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.