Evidence map›Paper›PMID 32158192›Full record

ArticleDrug design, development and therapy2020

Ox-LDL Causes Endothelial Cell Injury Through ASK1/NLRP3-Mediated Inflammasome Activation via Endoplasmic Reticulum Stress.

Liwei Hang, Yan Peng, Rui Xiang, Xiangdong Li, Zhiliang Li

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Drug design, development and therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing 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

38 citing papers in PubMed.

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  11. Endothelial-Protective Actions of Diethylether Extract fromInternational journal of molecular sciences · 2025
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  19. Lipotoxicity, ER Stress, and Cardiovascular Disease: Current Understanding and Future Directions.Cardiovascular & hematological agents in medicinal chemistry · 2024
    Review
  20. 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

5 authors.

Liwei Hang *Department of Cardiology, Heart Center, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, People's Republic of China.
Yan Peng *Department of Critical Care Medicine, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, People's Republic of China.
Rui XiangDepartment of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, People's Republic of China.
Xiangdong LiFuwai Hospital, National Center of Cardiovascular Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, People's Republic of China.ORCID 0000-0002-9227-5962
Zhiliang LiDepartment of Cardiology, Heart Center, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510280, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThis study was to investigate the mechanism of inflammatory pathology modification induced by ox-LDL in endothelial cells. METHODOLOGY: In this study, we firstly investigated the efflux of cholesterol of endothelial cells under the treatment of ox-LDL, and cell proliferation, ROS production, cell apoptosis was measured. Further, proteins of ASK1, NLRP3 inflammasomes and endoplasmic reticulum stress response were detected. Afterwards, ASK1 inhibitor (GS-4997) or endoplasmic reticulum stress (ERS) inhibitor (4-PBA) was used to measure the performance of endothelial cells.

resultsIn this study, endothelial cells were treated with ox-LDLs alone or in combination with a GS-4997 or 4-PBA. Results showed that ox-LDLs attenuated the efflux of cholesterol from endothelial cells in a dose-dependent manner. Ox-LDLs inhibited the proliferation of endothelial cells, and induced their apoptosis and production of reactive oxygen species (ROS). Additionally, ox-LDLs upregulated the levels of phosphorylated ASK1, ERS-related proteins (chop, p-PERK, GRP78, and p-IRE-1), and inflammation-associated proteins (NLRP3, IL-1β, and caspase 1) in endothelial cells. Moreover, we proved that GS-4997 could partly reverse ox-LDL-mediated cell proliferation, apoptosis, ROS production, and inflammation in endothelial cells, and increase cholesterol efflux. We also found that 4-PBA could attenuate the effects of ox-LDLs on endothelial cell cholesterol efflux, proliferation, apoptosis, ROS production, and inflammation.

conclusionOur results suggest that cholesterol efflux from endothelial cells is reduced by ox-LDLs, and these reductions in cholesterol efflux are accompanied by increased NLRP3 inflammasome signaling, ASK1 and higher levels of endoplasmic reticulum stress. Our results suggest this axis as potential targets for treating atherosclerosis.

Indexed as

Cell ProliferationCells, CulturedDose-Response Relationship, DrugEndoplasmic Reticulum Chaperone BiPEndoplasmic Reticulum StressEndothelial CellsHumansInflammasomesLipoproteins, LDLMAP Kinase Kinase Kinase 5NLR Family, Pyrin Domain-Containing 3 ProteinReactive Oxygen SpeciesEndoplasmic Reticulum Chaperone BiPHSPA5 protein, humanInflammasomesLipoproteins, LDLMAP3K5 protein, humanMAP Kinase Kinase Kinase 5NLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanoxidized low density lipoproteinReactive Oxygen Speciesapoptosis signal-regulating kinase 1cholesterol effluxendoplasmic reticulum stressendothelial cellinflammatory corpusclesox-LDL

Identifiers

PMID32158192
PMCPMC7047838

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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.