Evidence map›Paper›PMID 25313537›Full record

ArticleAntioxidants & redox signaling2015

Oxidized high-density lipoprotein impairs endothelial progenitor cells' function by activation of CD36-MAPK-TSP-1 pathways.

Jianxiang Wu, Zhiqing He, Xiang Gao, Feng Wu, Ru Ding, Yusheng Ren, Qijun Jiang, Min Fan, Chun Liang, Zonggui Wu

Open access · hybridAbstract read
In one paragraph

Article in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

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  11. Advances in HDL: Much More than Lipid Transporters.International journal of molecular sciences · 2020
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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

10 authors at 2 institutions in 2 countries.

Jianxiang Wu1 Department of Cardiology, Shanghai Changzheng Hospital, Second Military Medical University , Shanghai, People's Republic of China .
Zhiqing He
Xiang Gao
Feng Wu
Ru Ding
Yusheng Ren
Qijun Jiang
Min Fan
Chun Liang
Zonggui Wu
Second Military Medical University · CNBoston University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsHigh-density lipoprotein (HDL) levels inversely correlate with cardiovascular events due to the protective effects on vascular wall and stem cells, which are susceptible to oxidative modifications and then lead to potential pro-atherosclerotic effects. We proposed that oxidized HDL (ox-HDL) might lead to endothelial progenitor cells (EPCs) dysfunction and investigated underlying mechanisms.

resultsox-HDL was shown to increase apoptosis and intracellular reactive oxygen species levels, but to reduce migration, angiogenesis, and cholesterol efflux of EPCs in a dose-dependent manner. p38 mitogen-activated protein kinase (MAPK) and NF-κB were activated after ox-HDL stimulation, which also upregulated thrombospondin-1 (TSP-1) expression without affecting vascular endothelial growth factor. Effects caused by ox-HDL could be significantly attenuated by pretreatment with short hairpin RNA-mediated CD36 knockdown or probucol. Data of in vivo experiments and the inverse correlation of ox-HDL and circulating EPC numbers among patients with coronary artery diseases (CAD) or CAD and type 2 diabetes also supported it. Meanwhile, HDL separated from such patients could significantly increase cultured EPC's caspase 3 activity, further supporting our proposal. INNOVATION: This is the most complete study to date of how ox-HDL would impair EPCs function, which was involved with activation of CD36-p38 MAPK-TSP-1 pathways and proved by not only the inverse relationship between ox-HDL and circulating EPCs in clinic but also pro-apoptotic effects of HDL separated from patients' serum.

conclusionActivation of CD36-p38 MAPK-TSP-1 pathways contributes to the pathological effects of ox-HDL on EPCs' dysfunction, which might be one of the potential etiological factors responsible for the disturbed neovascularization in chronic ischemic disease.

Indexed as

MAP Kinase Signaling SystemAnimalsApoptosisBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCase-Control StudiesCD36 AntigensCell MovementCells, CulturedCholesterolCoronary Artery DiseaseDiabetes Mellitus, Type 2Endothelial Progenitor CellsFemaleGene ExpressionHindlimbHumansBasic Helix-Loop-Helix Leucine Zipper Transcription FactorsCD36 AntigensCholesterolLipoproteins, HDLNF-kappa BReactive Oxygen SpeciesSPZ1 protein, humanVascular Endothelial Growth Factor AVEGFA protein, human

Identifiers

PMID25313537
PMCPMC4298149
OpenAlexW2326830859

What OpenQuestion holds

Textmetadata
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 OpenQuestion graph.