Evidence map›Paper›PMID 36071548›Full record

ArticleJournal of cellular and molecular medicine2022

Macrophage-derived exosomal miR-4532 promotes endothelial cells injury by targeting SP1 and NF-κB P65 signalling activation.

Peng Liu, Shuya Wang, Guangxin Wang, Mingming Zhao, Fengli Du, Kaiyuan Li, Lei Wang, Huihui Wu, Jiamin Chen, Yang Yang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 2 pooled it
3.4field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 2 syntheses or guidelines pooled it, 41 citations in OpenAlex.

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  11. Circulating Extracellular Vesicles in Cardiovascular Disease.International journal of molecular sciences · 2025
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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

11 authors at 3 institutions in 1 country.

Peng LiuCentral Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Shuya WangCentral Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.ORCID 0000-0002-9360-9194
Guangxin WangCentral Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Mingming ZhaoResearch Center of Translational Medicine, Jinan Central Hospital, Cheeloo College Shandong University, Jinan, Shandong, China.
Fengli DuShandong Provincial Public Health Clinical Center, Jinan, Shandong, China.
Kaiyuan LiCentral Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Lei WangCentral Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Huihui WuResearch Center of Translational Medicine, Jinan Central Hospital, Cheeloo College Shandong University, Jinan, Shandong, China.
Jiamin ChenResearch Center of Translational Medicine, Jinan Central Hospital, Cheeloo College Shandong University, Jinan, Shandong, China.
Yang YangCentral Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Guohai SuCentral Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, China.
Jinan Central Hospital · CNShandong University · CNShanghai Public Health Clinical Center · CN

Funding

Natural Science Foundation of Shandong Province ZR202102220620Natural Science Foundation of Shandong Province ZR202103050087
6 · The paper itself

Abstract

Atherosclerosis is a complex pathological process involving macrophages, endothelial cells and vascular smooth muscle cells that can lead to ischemic heart disease; however, the mechanisms underlying cell-to-cell communication in atherosclerosis are poorly understood. In this study, we focused on the role of exosomal miRNAs in crosstalk between macrophages and endothelial cells and explored the rarely studied molecular mechanisms involved. Our in vitro result showed that macrophage-derived exosomal miR-4532 significantly disrupted human umbilical vein endothelial cells (HUVECs) function by targeting SP1 and downstream NF-κB P65 activation. In turn, increased endothelin-1 (ET-1), intercellular cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) and decreased endothelial nitric oxide synthase (eNOS) expression in HUVECs increased attraction of macrophages, exacerbating foam cell formation and transfer of exosomal miR-4532 to HUVECs. MiR-4532 overexpression significantly promoted endothelial injury and pretreatment with an inhibitor of miR-4532 or GW4869 (exosome inhibitor) could reverse this injury. In conclusion, our data reveal that exosomes have a critical role in crosstalk between HUVECs and macrophages. Further, exosomal miR-4532 transferred from macrophages to HUVECs and targeting specificity protein 1 (SP1) may be a novel therapeutic target in patients with atherosclerosis.

Indexed as

AtherosclerosisMicroRNAsSp1 Transcription FactorEndothelin-1ExosomesHumansHuman Umbilical Vein Endothelial CellsIntercellular Adhesion Molecule-1MacrophagesNF-kappa BNitric Oxide Synthase Type IIITranscription Factor RelAVascular Cell Adhesion Molecule-1Endothelin-1Intercellular Adhesion Molecule-1MicroRNAsNF-kappa BNitric Oxide Synthase Type IIIRELA protein, humanSP1 protein, humanSp1 Transcription FactorTranscription Factor RelAVascular Cell Adhesion Molecule-1atherosclerosisendothelial cellsexosomemacrophagesmiR-4532NF-κB P65SP1

Identifiers

PMID36071548
PMCPMC9575109
OpenAlexW4294991876

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.