Evidence map›Paper›PMID 22279032›Full record

ArticleDiabetes care2012

Effects of electronegative VLDL on endothelium damage in metabolic syndrome.

Chu-Huang Chen, Jonathan Lu, Shu-Hua Chen, Roger Y Huang, H Ramazan Yilmaz, Jianwen Dong, MacArthur A Elayda, Richard A F Dixon, Chao-Yuh Yang

Open access · hybridAbstract read
In one paragraph

Article in Diabetes care, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 37 citations in OpenAlex.

  1. Trial
  2. Article
  3. Very low-density lipoprotein and the human health.World journal of experimental medicine · 2026
    Review
  4. Cellular basis of HFpEF: contributions of abnormal lipids.Frontiers in cardiovascular medicine · 2026
    Review
  5. Up-regulated small-conductance calcium-activated potassium currents contribute to atrial arrhythmogenesis in high-fat feeding mice.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023
    Article
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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 2 institutions in 3 countries.

Chu-Huang ChenTexas Heart Institute, Houston, Texas, USA. cchen@heart.thi.tmc.edu
Jonathan Lu
Shu-Hua Chen
Roger Y Huang
H Ramazan Yilmaz
Jianwen Dong
MacArthur A Elayda
Richard A F Dixon
Chao-Yuh Yang
China Medical University Hospital · TWMevlana University · TR

Funding

Oxidation of Apolipoprotein B-100 in LDLR01HL063364 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI YANG, CHAO-YUH · 2001 to 2004
$1.2M
NHLBI NIH HHS HL-63364NHLBI NIH HHS R01 HL063364
6 · The paper itself

Abstract

objectiveBiochemical heterogeneity governs functional disparities among lipoproteins. We examined charge-defined VLDL subfractions in metabolic syndrome (MetS) to determine whether their increased electronegativity is associated with increased cytotoxicity and whether high concentrations of highly electronegative subfractions render VLDL harmful to the vascular endothelium. RESEARCH DESIGN AND

methodsPlasma VLDL of normal individuals (control subjects) (n = 13) and of those with MetS (n = 13) was resolved into subfractions with increasing negative charge (V1-V5) by anion-exchange chromatography. Human aortic endothelial cells were treated with V1-V5 or unfractionated VLDL.

resultsCompared with the control subjects, individuals with MetS had a significantly higher percentage of V5 VLDL (V5/VLDL%) (34 ± 20 vs. 39 ± 11%, respectively; P < 0.05) and plasma V5 concentration ([V5]) (5.5 ± 4.4 vs. 15.2 ± 8.5 mg/dL, respectively; P < 0.001). Apolipoprotein (apo)B100 levels decreased and apoC levels increased from V1 to V5, indicating that V5 is apoC-rich VLDL. Regression analyses of all 26 individuals showed that [V5] was positively correlated with total cholesterol (P = 0.016), triglyceride (P < 0.000001), and V5/VLDL% (P = 0.002). Fasting plasma glucose, but not waist circumference, exhibited a positive trend (P = 0.058); plasma HDL cholesterol exhibited a weak inverse trend (P = 0.138). V5 (10 μg/mL) induced apoptosis in ~50% of endothelial cells in 24 h. V5 was the most rapidly (<15 min) internalized subfraction and induced the production of reactive oxygen species (ROS) in endothelial cells after 20 min. Unfractionated MetS VLDL, but not control VLDL, also induced ROS production and endothelial cell apoptosis.

conclusionsIn populations with increased risk of diabetes, the vascular endothelium is constantly exposed to VLDL that contains a high proportion of V5. The potential impact of V5-rich VLDL warrants further investigation.

Indexed as

AdultCholesterol, VLDLEndothelium, VascularFemaleHumansLinear ModelsMaleMetabolic SyndromeMiddle AgedCholesterol, VLDL

Identifiers

PMID22279032
PMCPMC3322679
OpenAlexW2151307659

What OpenQuestion 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 OpenQuestion graph.