Evidence map›Paper›PMID 15660260›Full record

ArticleDiabetologia2005

Glycation of low-density lipoproteins by methylglyoxal and glycolaldehyde gives rise to the in vitro formation of lipid-laden cells.

B E Brown, R T Dean, M J Davies

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Diabetologia, 2005. 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
3.4field-weighted citation impact, top 7% 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, 77 citations in OpenAlex.

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  3. Does AGE-RAGE Stress Play a Role in the Development of Coronary Artery Disease in Obesity?The International journal of angiology : official publication of the International College of Angiology, Inc · 2022
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  6. AGE-RAGE Stress and Coronary Artery Disease.The International journal of angiology : official publication of the International College of Angiology, Inc · 2021
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  7. AGE-RAGE Axis in the Pathophysiology of Chronic Lower Limb Ischemia and a Novel Strategy for Its Treatment.The International journal of angiology : official publication of the International College of Angiology, Inc · 2020
    Review
  8. Article
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  11. AGE-RAGE Stress, Stressors, and Antistressors in Health and Disease.The International journal of angiology : official publication of the International College of Angiology, Inc · 2018
    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

3 authors at 2 institutions in 1 country.

B E BrownFree Radical Group, The Heart Research Institute, 145 Missenden Road, Camperdown, Sydney 2050, Australia.
R T Dean
M J Davies
The Heart Research Institute · AUUniversity of Canberra · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aims/hypothesisPrevious studies have implicated the glycoxidative modification of low-density lipoprotein (LDL) by glucose and aldehydes (apparently comprising both glycation and oxidation), as a causative factor in the elevated levels of atherosclerosis observed in diabetic patients. Such LDL modification can result in unregulated cellular accumulation of lipids. In previous studies we have characterized the formation of glycated, but nonoxidized, LDL by glucose and aldehydes; in this study we examine whether glycation of LDL, in the absence of oxidation, gives rise to lipid accumulation in arterial wall cell types.

methodsGlycated LDLs were incubated with macrophage, smooth muscle, or endothelial cells. Lipid loading was assessed by HPLC analysis of cholesterol and individual esters. Oxidation was assessed by cholesterol ester loss and 7-ketocholesterol formation. Cell viability was assessed by lactate dehydrogenase release and cell protein levels.

resultsGlycation of LDL by glycolaldehyde and methylglyoxal, but not glucose (in either the presence or absence of copper ions), resulted in cholesterol and cholesterol ester accumulation in macrophage cells, but not smooth muscle or endothelial cells. The extent of lipid accumulation depends on the degree of glycation, with increasing aldehyde concentration or incubation time, giving rise to greater extents of particle modification and lipid accumulation. Modification of lysine residues appears to be a key determinant of cellular uptake. CONCLUSIONS/

interpretationThese results are consistent with LDL glycation, in the absence of oxidation, being sufficient for rapid lipid accumulation by macrophage cells. Aldehyde-mediated "carbonyl-stress" may therefore facilitate the formation of lipid-laden (foam) cells in the artery wall.

Indexed as

AcetaldehydeAnimalsGlycated ProteinsGlycation End Products, AdvancedHumansIndicators and ReagentsLipoproteinsLipoproteins, LDLPyruvaldehydeRatsAcetaldehydeglycated lipoproteins, LDLGlycated ProteinsGlycation End Products, AdvancedglycolaldehydeIndicators and ReagentsLipoproteinsLipoproteins, LDLPyruvaldehyde

Identifiers

PMID15660260
OpenAlexW2057325586

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.