ArticleThe Journal of clinical investigation1997
Lipoprotein(a) vascular accumulation in mice. In vivo analysis of the role of lysine binding sites using recombinant adenovirus.
Article in The Journal of clinical investigation, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 68 citations in OpenAlex.
- The Roles of Lipoprotein(a) in Atherosclerosis - Minding the Knowledge Gaps.Current atherosclerosis reports · 2026Review
- Lipoprotein(a) and Heart Failure Among Black and White Participants in Atherosclerosis Risk in Communities Study, Framingham Offspring Study, and Multi-Ethnic Study of Atherosclerosis: The Pooling Project.Journal of the American Heart Association · 2025Article
- Lipoprotein(a) and panvascular disease.Lipids in health and disease · 2025Review
- Calcific aortic valve disease: from molecular and cellular mechanisms to medical therapy.European heart journal · 2022Article
- Lipoprotein(a): A Genetically Determined, Causal, and Prevalent Risk Factor for Atherosclerotic Cardiovascular Disease: A Scientific Statement From the American Heart Association.Arteriosclerosis, thrombosis, and vascular biology · 2022Review
- Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule.Journal of lipids · 2020Review
- Oxidized phospholipids as a unifying theory for lipoprotein(a) and cardiovascular disease.Nature reviews. Cardiology · 2019Review
- Race-Based Differences in Lipoprotein(a)-Associated Risk of Carotid Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- Lipoprotein(a) Associated Molecules are Prominent Components in Plasma and Valve Leaflets in Calcific Aortic Valve Stenosis.JACC. Basic to translational science · 2017Article
- Emerging Therapeutic Options for Lowering of Lipoprotein(a): Implications for Prevention of Cardiovascular Disease.Current atherosclerosis reports · 2016Review
- Structure, function, and genetics of lipoprotein (a).Journal of lipid research · 2016Review
- Lipoprotein(a) and oxidized phospholipids in calcific aortic valve stenosis.Current opinion in cardiology · 2016Review
- Production of human apolipoprotein(a) transgenic NIBS miniature pigs by somatic cell nuclear transfer.Experimental animals · 2016Article
- Mechanistic insights into Lp(a)-induced IL-8 expression: a role for oxidized phospholipid modification of apo(a).Journal of lipid research · 2015Article
- Determinants of binding of oxidized phospholipids on apolipoprotein (a) and lipoprotein (a).Journal of lipid research · 2013Article
- Lipoprotein(a) metabolism: potential sites for therapeutic targets.Metabolism: clinical and experimental · 2013Review
- Apolipoprotein(a) stimulates nuclear translocation of β-catenin: a novel pathogenic mechanism for lipoprotein(a).Molecular biology of the cell · 2013Article
- Lipoprotein(a) accelerates atherosclerosis in uremic mice.Journal of lipid research · 2010Article
- A physiological function for apolipoprotein(a): a natural regulator of the inflammatory response.Experimental biology and medicine (Maywood, N.J.) · 2009Article
- Apolipoprotein(a), through its strong lysine-binding site in KIV(10'), mediates increased endothelial cell contraction and permeability via a Rho/Rho kinase/MYPT1-dependent pathway.The Journal of biological chemistry · 2008Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Although the mechanism by which lipoprotein(a) [Lp(a)] contributes to vascular disease remains unclear, consequences of its binding to the vessel surface are commonly cited in postulated atherogenic pathways. Because of the presence of plasminogen-like lysine binding sites (LBS) in apo(a), fibrin binding has been proposed to play an important role in Lp(a)'s vascular accumulation. Indeed, LBS are known to facilitate Lp(a) fibrin binding in vitro. To examine the importance of apo(a) LBS in Lp(a) vascular accumulation in vivo, we generated three different apo(a) cDNAs: (a) mini apo(a), based on wild-type human apo(a); (b) mini apo(a) containing a naturally occurring LBS defect associated with a point mutation in kringle 4-10; and (c) human- rhesus monkey chimeric mini apo(a), which contains the same LBS defect in the context of several additional changes. Recombinant adenovirus vectors were constructed with the various apo(a) cDNAs and injected into human apoB transgenic mice. At the viral dosage used in these experiments, all three forms of apo(a) were found exclusively within the lipoprotein fractions, and peak Lp(a) plasma levels were nearly identical (approximately 45 mg/dl). In vitro analysis of Lp(a) isolated from the various groups of mice confirmed that putative LBS defective apo(a) yielded Lp(a) unable to bind lysine-Sepharose. Quantitation of in vivo Lp(a) vascular accumulation in mice treated with the various adenovirus vectors revealed significantly less accumulation of both types of LBS defective Lp(a), relative to wild-type Lp(a). These results indicate a correlation between lysine binding properties of Lp(a) and vascular accumulation, supporting the postulated role of apo(a) LBS in this potentially atherogenic characteristic of Lp(a).
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Registered trials
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.