Evidence map›Paper›PMID 38870781›Full record

ArticleRedox biology2024

Activation of Nrf2 inhibits atherosclerosis in ApoE

Lei He, Qinghua Chen, Li Wang, Yujie Pu, Juan Huang, Chak Kwong Cheng, Jiang-Yun Luo, Lijing Kang, Xiao Lin, Li Xiang and 8 more

Abstract read
In one paragraph

Article in Redox biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing 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

32 citing papers in PubMed.

  1. Hepatocyte-SpecificAntioxidants (Basel, Switzerland) · 2026
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  15. Article
  16. Review
  17. Endothelial Metabolic Reprogramming Links Diabetes to Atherosclerosis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026
    Review
  18. Article
  19. Article
  20. Article
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

18 authors.

Lei HeDepartment of Biomedical Sciences, City University of Hong Kong, Hong Kong, PR China; School of Biomedical Sciences, Chinese University of Hong Kong, Hong Kong, PR China.
Qinghua ChenDepartment of Biomedical Sciences, City University of Hong Kong, Hong Kong, PR China.
Li WangDepartment of Biomedical Sciences, City University of Hong Kong, Hong Kong, PR China.
Yujie PuDepartment of Biomedical Sciences, City University of Hong Kong, Hong Kong, PR China.
Juan HuangSchool of Biomedical Sciences, Chinese University of Hong Kong, Hong Kong, PR China; Shenzhen Key Laboratory of Cardiovascular Disease, Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen, PR China.
Chak Kwong ChengDepartment of Biomedical Sciences, City University of Hong Kong, Hong Kong, PR China.
Jiang-Yun LuoSchool of Biomedical Sciences, Chinese University of Hong Kong, Hong Kong, PR China.
Lijing KangDepartment of Biomedical Sciences, City University of Hong Kong, Hong Kong, PR China.
Xiao LinDepartment of Psychiatry, Icahn School of Medicine at Mount Sinai, New York, USA.
Li XiangState Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong, PR China.
Liang FangDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
Ben HeDepartment of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, PR China.
Yin XiaSchool of Biomedical Sciences, Chinese University of Hong Kong, Hong Kong, PR China.
Kathy O LuiDepartment of Chemical Pathology, and Li Ka Shing Institute of Health Science, The Chinese University of Hong Kong, Hong Kong, PR China.
Yong PanDepartment of Pathophysiology, School of Basic Medical Sciences, Shenzhen University Medical School, Shenzhen, PR China.
Jie LiuDepartment of Pathophysiology, School of Basic Medical Sciences, Shenzhen University Medical School, Shenzhen, PR China.
Cheng-Lin ZhangDepartment of Pathophysiology, School of Basic Medical Sciences, Shenzhen University Medical School, Shenzhen, PR China. Electronic address: zhangchenglin07@szu.edu.cn.
Yu HuangDepartment of Biomedical Sciences, City University of Hong Kong, Hong Kong, PR China; School of Biomedical Sciences, Chinese University of Hong Kong, Hong Kong, PR China. Electronic address: yu.huang@cityu.edu.hk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNuclear erythroid 2-related factor 2 (Nrf2), a transcription factor, is critically involved in the regulation of oxidative stress and inflammation. However, the role of endothelial Nrf2 in atherogenesis has yet to be defined. In addition, how endothelial Nrf2 is activated and whether Nrf2 can be targeted for the prevention and treatment of atherosclerosis is not explored.

methodsRNA-sequencing and single-cell RNA sequencing analysis of mouse atherosclerotic aortas were used to identify the differentially expressed genes. In vivo endothelial cell (EC)-specific activation of Nrf2 was achieved by injecting adeno-associated viruses into ApoE

resultsEndothelial inflammation appeared as early as on day 3 after feeding of a high cholesterol diet (HCD) in ApoE

conclusionsUpon HCD feeding in ApoE

Indexed as

Apolipoproteins EAtherosclerosisEndothelial CellsInflammationLipid PeroxidationNF-E2-Related Factor 2AnimalsDisease Models, AnimalHumansMaleMiceMice, KnockoutOxidative StressApoe protein, mouseApolipoproteins ENfe2l2 protein, mouseNF-E2-Related Factor 2AtherosclerosisEndothelial cellsInflammationLipid peroxidationNuclear erythroid 2-related factor 2

Identifiers

PMID38870781
PMCPMC11247299

What OpenQuestion holds

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Registered trials

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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.