Evidence map›Paper›PMID 39985585›Full record

ArticleCellular and molecular life sciences : CMLS2025

NR4A1 deficiency promotes carotid plaque vulnerability by activating integrated stress response via targeting Bcat1.

Long Chen, Yiping Shi, Danrui Xiao, Yijie Huang, Yangjing Jiang, Min Liang, Feng Liang, Jieyuan Xue, Haiping Chen, Zhitong Liu and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2025. 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

17 authors.

Long Chen *Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Yiping Shi *Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Danrui Xiao *Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Yijie Huang *Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Yangjing JiangDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Min LiangDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Feng LiangDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Jieyuan XueDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Haiping ChenDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Zhitong LiuDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Xia WangDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Fei ZhuangDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Guo ZhouDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Huanhuan HuoDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.
Zhaohua CaiDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China. zcai5@yahoo.com.
Qin ShaoDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China. shaoqindr@126.com.
Ben HeDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China. heben@shchest.org.ORCID http://orcid.org/0000-0002-6717-9039

Funding

National Natural Science Foundation of China 81870338the National Natural Science Foundation of China 82300489The National Natural Science Foundation of China 82130012
6 · The paper itself

Abstract

Rupture of vulnerable carotid atherosclerotic plaque is one of the leading causes of ischemic stroke. However, the mechanisms driving the transition from stable to vulnerable plaques have not yet been elucidated. NR4A1 is an orphan nuclear receptor that functions in various inflammatory diseases. To explore the role of NR4A1 in vulnerable plaque formation, we generated a vulnerable plaque mouse model by combining partial ligation of the left common carotid artery and left renal artery in ApoE

Indexed as

Nuclear Receptor Subfamily 4, Group A, Member 1Plaque, AtheroscleroticAnimalsApolipoproteins EDisease Models, AnimalHumansInflammationMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutOxidative StressApolipoproteins ENr4a1 protein, mouseNuclear Receptor Subfamily 4, Group A, Member 1Bcat1Integrated stress responseNR4A1Vulnerable plaque

Identifiers

PMID39985585
PMCPMC11846829

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.