Evidence map›Paper›PMID 29695496›Full record

ArticleBioscience reports2018

oxLDL-mediated cellular senescence is associated with increased NADPH oxidase p47phox recruitment to caveolae.

Jing Wang, Yuzhi Bai, Xia Zhao, Jing Ru, Ning Kang, Tian Tian, Liying Tang, Yun An, Pei Li

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 15% of its field
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

24 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  9. Association ofPeerJ · 2024
    Article
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  11. New insight into dyslipidemia-induced cellular senescence in atherosclerosis.Biological reviews of the Cambridge Philosophical Society · 2022
    Review
  12. Review
  13. Review
  14. Article
  15. Oxidized LDLs as Signaling Molecules.Antioxidants (Basel, Switzerland) · 2021
    Review
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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

9 authors at 3 institutions in 1 country.

Jing WangDepartment of Geriatrics, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Yuzhi BaiDepartment of Geriatrics, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Xia ZhaoDepartment of Geriatrics, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Jing RuDepartment of Geriatrics, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Ning KangInstitute for Immunology, Department of Basic Medical Sciences, School of Medicine, Tsinghua-Peking Joint Center for Life Sciences, Tsinghua University, Beijing 100084, China.
Tian TianDepartment of Geriatrics, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Liying TangDepartment of Geriatrics, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Yun AnDepartment of Geriatrics, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100043, China.
Pei LiDepartment of Geriatrics, Beijing Chaoyang Hospital Affiliated to Capital Medical University, Beijing 100043, China lipei2231@126.com.
Beijing Chao-Yang Hospital · CNCapital Medical University · CNCenter for Life Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis develops as a consequence of inflammation and cell senescence. In critical factors involved in the atherosclerotic changes, reactive oxygen species (ROS) generation is considered a leading cause. While NADPH oxidases, particularly NOX2, are the main sources of ROS, how they are regulated in the disease is incompletely understood. In addition, how caveolae, the membrane structure implicated in oxLDL deposition under vascular endothelia, is involved in the oxLDL-mediated ROS production remains mostly elusive. We report here that macrophages exposed to oxLDL up-regulate its caveolin-1 expression, and the latter in turn up-regulates NOX2 p47phox level. This combination effect results in increased cellular senescence. Interestingly, oxLDL treatment causes the p47phox residing in the cytosol to translocate to the caveolae. Immunoprecipitation assays confirms that cavelin-1 is in high degree association with p47phox. These results suggest caveolin-1 may serve as the membrane target for p47phox and as a switch for ROS production following oxLDL exposure. Our results reveal a previously unknown molecular event in oxLDL-mediated cellular ageing, and may provide a target for clinical intervention for atherosclerosis.

Indexed as

AnimalsCaveolaeCaveolin 1Cellular SenescenceCytosolGene Expression RegulationHEK293 CellsHumansLipoproteins, LDLMiceNADPH OxidasesOxidation-ReductionProtein TransportRAW 264.7 CellsReactive Oxygen SpeciesRNA, Small InterferingCav1 protein, mouseCaveolin 1Lipoproteins, LDLNADPH Oxidasesneutrophil cytosolic factor 1oxidized low density lipoproteinReactive Oxygen SpeciesRNA, Small Interferingatherosclerosiscaveolin-1cell senescencep47phox

Identifiers

PMID29695496
PMCPMC5997791
OpenAlexW2801045454

What OpenQuestion holds

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LicenceCC BY
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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.