ArticleThe Journal of clinical investigation1996
Preferential influx and decreased fractional loss of lipoprotein(a) in atherosclerotic compared with nonlesioned rabbit aorta.
Article in The Journal of clinical investigation, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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.
Who cites it
14 citing papers in PubMed.
- Lipoprotein(a) and Cardiovascular Disease: From Genetic Risk Factor to Therapeutic Target.Cells · 2026Review
- Low-density lipoproteins cause atherosclerotic cardiovascular disease: pathophysiological, genetic, and therapeutic insights: a consensus statement from the European Atherosclerosis Society Consensus Panel.European heart journal · 2020 · on this mapArticle
- Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule.Journal of lipids · 2020Review
- Lipoprotein (a) as a cause of cardiovascular disease: insights from epidemiology, genetics, and biology.Journal of lipid research · 2016Review
- Production of human apolipoprotein(a) transgenic NIBS miniature pigs by somatic cell nuclear transfer.Experimental animals · 2016Article
- Coronary Artery Disease Severity and Cardiovascular Biomarkers in Patients with Peripheral Artery Disease.The International journal of angiology : official publication of the International College of Angiology, Inc · 2015Article
- Article
- Lipoprotein(a) metabolism: potential sites for therapeutic targets.Metabolism: clinical and experimental · 2013Review
- Lipoprotein(a) accelerates atherosclerosis in uremic mice.Journal of lipid research · 2010Article
- Human stanniocalcin-1 blocks TNF-alpha-induced monolayer permeability in human coronary artery endothelial cells.Arteriosclerosis, thrombosis, and vascular biology · 2008Article
- Lipoprotein(a): biology and clinical importance.The Clinical biochemist. Reviews · 2004Article
- Glycosaminoglycan-lipoprotein interaction.Glycoconjugate journal · 2001Article
- Lipoprotein(a) vascular accumulation in mice. In vivo analysis of the role of lysine binding sites using recombinant adenovirus.The Journal of clinical investigation · 1997Article
- Susceptibility to atherosclerosis in mice expressing exclusively apolipoprotein B48 or apolipoprotein B100.The Journal of clinical investigation · 1997Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim was to investigate the atherogenic potential of lipoprotein(a) (Lp(a)) and to further our understanding of the atherogenic process by measuring rates of transfer into the intima-inner media (i.e., intimal clearance) and rates of loss from the intima-inner media (i.e., fractional loss) of Lp(a) and LDL using cholesterol-fed rabbits with nonlesioned (n = 13) or atherosclerotic aortas (n = 12). In each rabbit, 131I-Lp(a) (or 131I-LDL) was injected intravenously 26 h before and 125I-Lp(a) (or 125I-LDL) 3 h before the aorta was removed and divided into six consecutive segments of similar size. The intimal clearance of Lp(a) and LDL was similar and markedly increased in atherosclerotic compared with nonlesioned aortas (ANOVA, effect of atherosclerosis: P < 0.0001). Fractional losses of labeled Lp(a) and labeled LDL in atherosclerotic aorta were on average 25 and 43%, respectively, of that in nonlesioned aortas (ANOVA, effect of atherosclerosis: P < 0.0001). Fractional loss of Lp(a) was 73% of that of LDL (ANOVA, effect of type of lipoprotein: P = 0.07). These data suggest that the development of atherosclerosis is associated with increased influx as well as decreased fractional loss of Lp(a) and LDL from the intima. Accordingly, Lp(a) may share with LDL the potential for causing atherosclerosis.
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Registered trials
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