ArticleThe Journal of clinical investigation1997
The atherogenic lipoprotein Lp(a) is internalized and degraded in a process mediated by the VLDL receptor.
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 42 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
42 citing papers in PubMed, 175 citations in OpenAlex.
- Association of Serum Lipoprotein (a) Levels and Coronary Atheroma Volume by Intravascular Ultrasound.Journal of the American Heart Association · 2020Trial
- Metabolic effects of PCSK9 inhibition with Evolocumab in subjects with elevated Lp(a).Lipids in health and disease · 2020Trial
- Lipoprotein(a) in Coronary Artery Disease and Aortic Stenosis: Pathophysiology, Clinical Impact, Interventional Implications and Emerging Targeted Therapies.Journal of clinical medicine · 2026Review
- Diabetes Mellitus and Lipoprotein(a): A Determinant Interaction in Micro- and Macrovascular Damage.International journal of molecular sciences · 2025Review
- Functional interrogation of cellular Lp(a) uptake by genome-scale CRISPR screening.Atherosclerosis · 2025Article
- Interaction Between Lipoprotein(a) and Other Lipid Molecules: A Review of the Current Literature.Biomolecules · 2025Review
- LDL atherogenicity determined by size, density, oxidation, apolipoprotein(a), and electronegativity: an updated review.Frontiers in cardiovascular medicine · 2025Review
- Lipids and Inflammation: Novel Molecular Targets and Therapeutic Implications.Current medicinal chemistry · 2025Review
- Lipoprotein (a): Underrecognized Risk with a Promising Future.Reviews in cardiovascular medicine · 2024Review
- Comparative Analysis of Atherogenic Lipoproteins L5 and Lp(a) in Atherosclerotic Cardiovascular Disease.Current atherosclerosis reports · 2024Review
- Haplotype of the Lipoprotein(a) Gene Variants rs10455872 and rs3798220 Is Associated with Parameters of Coagulation, Fibrinolysis, and Inflammation in Patients after Myocardial Infarction and Highly Elevated Lipoprotein(a) Values.International journal of molecular sciences · 2024Article
- Sortilin enhances secretion of apolipoprotein(a) through effects on apolipoprotein B secretion and promotes uptake of lipoprotein(a).Journal of lipid research · 2022Article
- Lipoprotein (a): When to Measure and How to Treat?Current atherosclerosis reports · 2021Review
- Metabolic syndrome, lipoprotein(a) and subclinical atherosclerosis in Mexican populationArchivos de cardiologia de Mexico · 2021Article
- Recent Updates of Lipoprotein(a) and Cardiovascular Disease.Chonnam medical journal · 2021Review
- Lipoprotein(a) in atherosclerosis: from pathophysiology to clinical relevance and treatment options.Annals of medicine · 2020 · on this mapReview
- Lipoprotein receptor signalling in atherosclerosis.Cardiovascular research · 2020Review
- Pragmatic Analysis of Dyslipidemia Involvement in Coronary Artery Disease: A Narrative Review.Current cardiology reviews · 2020Review
- Consumption of a defined, plant-based diet reduces lipoprotein(a), inflammation, and other atherogenic lipoproteins and particles within 4 weeks.Clinical cardiology · 2018Article
- Triglyceride Rich Lipoprotein -LPL-VLDL Receptor and Lp(a)-VLDL Receptor Pathways for Macrophage Foam Cell Formation.Journal of atherosclerosis and thrombosis · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Lp(a) is a major inherited risk factor associated with premature heart disease and stroke. The mechanism of Lp(a) atherogenicity has not been elucidated, but likely involves both its ability to influence plasminogen activation as well as its atherogenic potential as a lipoprotein particle after receptor-mediated uptake. We demonstrate that fibroblasts expressing the human VLDL receptor can mediate endocytosis of Lp(a), leading to its degradation within lysosomes. In contrast, fibroblasts deficient in this receptor are not effective in catabolizing Lp(a). Lp(a) degradation was prevented by antibodies against the VLDL receptor, and by RAP, an antagonist of ligand binding to the VLDL receptor. Catabolism of Lp(a) was inhibited by apolipoprotein(a), but not by LDL or by monoclonal antibodies against apoB100 that block LDL binding to the LDL receptor, indicating that apolipoprotein(a) mediates Lp(a) binding to this receptor. Removal of Lp(a) antigen from the mouse circulation was delayed in mice deficient in the VLDL receptor when compared with control mice, indicating that the VLDL receptor may play an important role in Lp(a) catabolism in vivo. We also demonstrate the expression of the VLDL receptor in macrophages present in human atherosclerotic lesions. The ability of the VLDL receptor to mediate endocytosis of Lp(a) could lead to cellular accumulation of lipid within macrophages, and may represent a molecular basis for the atherogenic effects of Lp(a).
Indexed as
Identifiers
What OpenQuestion holds
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.