Evidence map›Paper›PMID 42436514›Full record

ArticleJournal of translational medicine2026

Macrophage extracellular traps accelerate atherosclerosis progression via Rap1 pathway-mediated necroptosis and phenotypic switching in vascular smooth muscle cells.

Suli Wang, Yajing Tang, Xinyi Yu, Zhenxing Liang, Dashuai Wang, Mingjie Xie, Liangjing Lu, Hai Liu

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of translational medicine, 2026. 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. Review
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

8 authors.

Suli Wang *Department of Rheumatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai, 200001, China.
Yajing Tang *Department of Cardiovascular Surgery, The Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.
Xinyi YuDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Road, Zhengzhou, 450052, China.
Zhenxing LiangDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Road, Zhengzhou, 450052, China.
Dashuai WangDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Road, Zhengzhou, 450052, China.
Mingjie XieDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Road, Zhengzhou, 450052, China.
Liangjing LuDepartment of Rheumatology, Renji Hospital, School of Medicine, Shanghai Jiao Tong University, 145 Middle Shandong Road, Shanghai, 200001, China. lu_liangjing@163.com.
Hai LiuDepartment of Cardiovascular Surgery, The First Affiliated Hospital of Zhengzhou University, No. 1 Jianshe East Road, Zhengzhou, 450052, China. fccliuh3@zzu.edu.cn.

Funding

National Key Research and Development Programme of China 2022YFC2504601Shanghai Pujiang Young Rheumatologists Training Program SPROG202008The National Natural Science Foundation of China 81500260the Scientific and Technological Research Project of Henan Province 242102310156
6 · The paper itself

Abstract

backgroundAtherosclerosis (AS) is a primary driver of cardiovascular diseases, with vascular smooth muscle cell (VSMC) fate being critical for plaque stability. Macrophage extracellular traps (METs) are implicated in AS, but their precise impact on VSMCs remains unclear. This study investigated the role of METs in VSMC necroptosis, phenotypic switching, and AS progression.

methodAn ApoE

resultsExogenous METs administration exacerbated AS plaque burden in ApoE

conclusionOur findings demonstrate that METs are endocytosed by VSMCs, activating the Rap1-MEK5-ERK5/p38 cascade to drive necroptosis and synthetic phenotypic transition, thereby accelerating AS progression. These insights provide a molecular foundation for developing novel therapies targeting METs or the Rap1 pathway to stabilize vulnerable plaques.

Indexed as

AtherosclerosisDisease ProgressionMacrophagesMuscle, Smooth, VascularMyocytes, Smooth MuscleNecroptosisrap1 GTP-Binding ProteinsSignal TransductionAnimalsApolipoproteins EMaleMiceMice, Inbred C57BLPhenotypePlaque, AtheroscleroticApolipoproteins Erap1 GTP-Binding ProteinsRap1 protein, mouseAtherosclerosisMacrophage extracellular trapsNecroptosisRap1Vascular smooth muscle cell

Identifiers

PMID42436514
PMCPMC13644069

What OpenQuestion holds

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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.