ArticleThe Journal of clinical investigation1997
Modification of apolipoprotein(a) lysine binding site reduces atherosclerosis in transgenic mice.
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 25 papers.
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.
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
25 citing papers in PubMed, 86 citations in OpenAlex.
- Presumed Mechanisms Underlying Lipoprotein(a)-caused Atherosclerosis.European cardiology · 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
- Comparative Analysis of Atherogenic Lipoproteins L5 and Lp(a) in Atherosclerotic Cardiovascular Disease.Current atherosclerosis reports · 2024Review
- High lipoprotein(a): Actionable strategies for risk assessment and mitigation.American journal of preventive cardiology · 2024Review
- Connecting impaired fibrinolysis and dyslipidemia.Research and practice in thrombosis and haemostasis · 2024Article
- Association of Lp(a) (Lipoprotein[a]) and Hypertension in Primary Prevention of Cardiovascular Disease: The MESA.Hypertension (Dallas, Tex. : 1979) · 2023Article
- Lipoprotein(a) in Atherosclerotic Diseases: From Pathophysiology to Diagnosis and Treatment.Molecules (Basel, Switzerland) · 2023Review
- 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): When to Measure and How to Treat?Current atherosclerosis reports · 2021Review
- Identification and analyses of inhibitors targeting apolipoprotein(a) kringle domains KIV-7, KIV-10, and KV provide insight into kringle domain function.The Journal of biological chemistry · 2020Article
- 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
- Apolipoprotein(a) Kringle-IV Type 2 Copy Number Variation Is Associated with Venous Thromboembolism.PloS one · 2016Article
- Determinants of binding of oxidized phospholipids on apolipoprotein (a) and lipoprotein (a).Journal of lipid research · 2013Article
- Lipoprotein(a) and cardiovascular disease in diabetic patients.Clinical lipidology · 2012Article
- Lipoprotein(a) as a cardiovascular risk factor: current status.European heart journal · 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
- Lipoprotein(a): new insights into mechanisms of atherogenesis and thrombosis.Clinical cardiology · 2004Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Lipoprotein(a) contributes to the development of atherosclerosis through the binding of its plasminogen-like apolipoprotein(a) component to fibrin and other plasminogen substrates. Apolipoprotein(a) contains a major lysine binding site in one of its kringle domains. Destruction of this site by mutagenesis greatly reduces the binding of apolipoprotein(a) to lysine and fibrin. Transgenic mice expressing this mutant form of apolipoprotein(a) as well as mice expressing wild-type apolipoprotein(a) have been created in an inbred mouse strain. The wild-type apolipoprotein(a) transgenic mice have a fivefold increase in the development of lipid lesions, as well as a large increase in the focal deposition of apolipoprotein(a) in the aorta, compared with the lysine binding site mutant strain and to nontransgenic littermates. The results demonstrate the key role of this lysine binding site in the pathogenic activity of apolipoprotein(a) in a murine model system.
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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.