Evidence map›Paper›PMID 42898474›Full record

ArticleResearch (Washington, D.C.)2026

Neutrophil Extracellular Traps-Mediated Intraplaque Angiogenesis and Microvascular Permeability Promote Rapid Plaque Progression following Myocardial Infarction.

Zhijun Lei, Yunfei Yin, Long Zeng, Na Yang, Ming Zhai, Yanxi Zeng, Yefei Shi, Qing Yu, Shiyu Gong, Weixia Jian and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Research (Washington, D.C.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Zhijun LeiDepartment of Cardiology, Shanghai Tenth People's Hospital , Tongji University School of Medicine, Shanghai, China.
Yunfei YinDepartment of Cardiology, Shanghai Tenth People's Hospital , Tongji University School of Medicine, Shanghai, China.
Long ZengDepartment of Cardiology, Shanghai Tenth People's Hospital , Tongji University School of Medicine, Shanghai, China.
Na YangDepartment of Cardiology, Shanghai Tenth People's Hospital , Tongji University School of Medicine, Shanghai, China.
Ming ZhaiDepartment of Cardiology, Shanghai Tenth People's Hospital , Tongji University School of Medicine, Shanghai, China.
Yanxi ZengDepartment of Cardiology, Shanghai Tenth People's Hospital , Tongji University School of Medicine, Shanghai, China.
Yefei ShiDepartment of Cardiology, Shanghai Tenth People's Hospital , Tongji University School of Medicine, Shanghai, China.
Qing YuDepartment of Cardiology, Shanghai Tenth People's Hospital , Tongji University School of Medicine, Shanghai, China.
Shiyu GongDepartment of Cardiology, Shanghai Tenth People's Hospital , Tongji University School of Medicine, Shanghai, China.
Weixia JianDepartment of Endocrinology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Jianhui ZhuangDepartment of Cardiology, Shanghai Tenth People's Hospital , Tongji University School of Medicine, Shanghai, China.
Li ZhangDepartment of Cardiology, Xinhua Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, China.
Wenhui PengDepartment of Cardiology, Shanghai Tenth People's Hospital , Tongji University School of Medicine, Shanghai, China.ORCID https://orcid.org/0000-0003-2937-0024

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite adherence to guideline-recommended therapies, survivors of myocardial infarction (MI) remain at high risk for recurrent ischemic events. This study aimed to elucidate the underlying mechanisms responsible for this residual risk. Using Mendelian randomization analysis and retrospective cohort study, we established a causal relationship between MI and plaque progression, potentially mediated by neutrophils. In a murine atherosclerotic model, MI precipitated a marked expansion in plaque volume accompanied by reduced stability; these pathological changes are consistent with the hallmark features of rapid plaque progression, which may trigger recurrent ischemic events. Pharmacological inhibition and adoptive transfer experiments using

Identifiers

PMID42898474
PMCPMC13678088

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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.