Evidence map›Paper›PMID 39838385›Full record

ArticleBMC biology2025

Endothelial cells under disturbed flow release extracellular vesicles to promote inflammatory polarization of macrophages and accelerate atherosclerosis.

Zhe Hou, Li Deng, Fei Fang, Ting Zhao, Yaojia Zhang, Gang Li, Michael Z Miao, Yongcang Zhang, Hongchi Yu, Xiaoheng Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
–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

13 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  12. Maladaptive trained immunity in viral infections.The Journal of clinical investigation · 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

10 authors.

Zhe Hou *Institute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Li Deng *Institute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Fei FangInstitute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Ting ZhaoInstitute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Yaojia ZhangInstitute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, 610041, China.
Gang LiDepartment of Genome Sciences, University of Washington, William H. Foege Hall, 3720 15 Ave NE, Seattle, 98195, USA.
Michael Z MiaoDivision of Oral & Craniofacial Health Sciences, University of North Carolina Adams School of Dentistry, Chapel Hill, NC, 27599, USA.
Yongcang ZhangMedical College, Tibet University, Lhasa, 850000, China.
Hongchi YuInstitute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, 610041, China. yuhongchi@scu.edu.cn.
Xiaoheng LiuInstitute of Biomedical Engineering, West China School of Basic Medical Sciences & Forensic Medicine, Sichuan University, Chengdu, 610041, China. liuxiaohg@scu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundExtracellular vesicles (EVs) derived from endothelial cells (ECs) are increasingly recognized for their role in the initiation and progression of atherosclerosis. ECs experience varying degrees and types of blood flow depending on their specific arterial locations. In regions of disturbed flow, which are predominant sites for atherosclerotic plaque formation, the impact of disturbed flow on the secretion and function of ECs-derived EVs remains unclear. This study aims to assess the role of disturbed flow in the secretion of EVs from ECs and to evaluate their proatherogenic function.

resultsOur comprehensive experiments revealed that disturbed flow facilitated the secretion of ECs-derived EVs both in vivo and in vitro. Mechanistically, the MAPK pathway transduces mechanical cues from disturbed flow in ECs, leading to increased secretion of EVs. Pharmacological inhibition of the MAPK pathway reduced the secretion of EVs even under disturbed flow conditions. Interestingly, under disturbed flow stimulation, ECs-derived EVs promoted monocyte accumulation and enhanced their invasion of the endothelium. More important, these EVs initiated the inflammatory polarization of macrophages from the M2 to the M1 phenotype. However, the phenotypic switching of vascular smooth muscle cells was not affected by exposure to these EVs.

conclusionsTaken together, targeting the MAPK signaling pathway holds potential as a novel therapeutic strategy for inhibiting the secretion of EC-derived EVs and mitigating the inflammatory polarization of macrophages, ultimately ameliorating the progression of atherosclerosis.

Indexed as

AtherosclerosisEndothelial CellsExtracellular VesiclesInflammationMacrophagesAnimalsHumansMaleMiceMice, Inbred C57BLAtherosclerosisDisturbed flowEndothelial cellsExtracellular vesicleMacrophages

Identifiers

PMID39838385
PMCPMC11753076

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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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 Socratic graph.