ArticleThe Biochemical journal2003
Galactose-specific asialoglycoprotein receptor is involved in lipoprotein (a) catabolism.
Article in The Biochemical journal, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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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.
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Who cites it
20 citing papers in PubMed, 61 citations in OpenAlex.
- A Position Paper on Lipoprotein(a) From the Lipoprotein(a) Task Force of the Korean Society of Lipid and Atherosclerosis: Current Evidence, Clinical Applications, and Future Directions.Journal of lipid and atherosclerosis · 2026Review
- A Position Paper on Lipoprotein(a) From the Lipoprotein(a) Task Force of the Korean Society of Lipid and Atherosclerosis: Current Evidence, Clinical Applications, and Future Directions.Korean circulation journal · 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
- ASGR1 Deficiency Inhibits Atherosclerosis in Western Diet-FedArteriosclerosis, thrombosis, and vascular biology · 2024Article
- Lipoprotein(a) as a Risk Factor for Cardiovascular Diseases: Pathophysiology and Treatment Perspectives.International journal of environmental research and public health · 2023Review
- Torularhodin Alleviates Hepatic Dyslipidemia and Inflammations in High-Fat Diet-Induced Obese Mice via PPARα Signaling Pathway.Molecules (Basel, Switzerland) · 2022Article
- Lp(a) and the Risk for Cardiovascular Disease: Focus on the Lp(a) Paradox in Diabetes Mellitus.International journal of molecular sciences · 2022Review
- Hypomorphic ASGR1 modulates lipid homeostasis via INSIG1-mediated SREBP signaling suppression.JCI insight · 2021Article
- Cell release during perfusion reflects cold ischemic injury in rat livers.Scientific reports · 2020Article
- 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 an Old and New Causal Risk Factor of Atherosclerotic Cardiovascular Disease.Journal of atherosclerosis and thrombosis · 2019 · on this mapReview
- Lipoprotein (a): a historical appraisal.Journal of lipid research · 2017Review
- ASGR1 - a new target for lowering non-HDL cholesterol.Global cardiology science & practice · 2016Article
- Lipoprotein (a) upregulates ABCA1 in liver cells via scavenger receptor-B1 through its oxidized phospholipids.Journal of lipid research · 2015Article
- HDL-C, ABCA1-mediated cholesterol efflux, and lipoprotein(a): insights into a potential novel physiologic role of lipoprotein(a).Journal of lipid research · 2015Article
- Lipoprotein(a) metabolism: potential sites for therapeutic targets.Metabolism: clinical and experimental · 2013Review
- Lipoprotein(a): an elusive cardiovascular risk factor.Arteriosclerosis, thrombosis, and vascular biology · 2004Review
- Lipoprotein(a): biology and clinical importance.The Clinical biochemist. Reviews · 2004Article
- The role of Lipoprotein(a) in cardiovascular disease: Current concepts and future perspectives.Hellenic journal of cardiology : HJC = Hellenike kardiologike epitheoreseReview
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lp(a) [lipoprotein (a)] is a highly atherogenic plasma lipoprotein assembled from low-density lipoprotein and the glycoprotein apolipoprotein (a). The rate of Lp(a) biosynthesis correlates significantly with plasma Lp(a) concentrations, whereas the fractional catabolic rate does not have much influence. So far, little is known about Lp(a) catabolism. To study the site and mode of Lp(a) catabolism, native or sialidase-treated Lp(a) was injected into hedgehogs or ASGPR (asialoglycoprotein receptor)-knockout (ASGPR-) mice or wild-type (ASGPR+) mice, and the decay of the plasma Lp(a) concentration was followed. COS-7 cells were transfected with high- (HL-1) and low-molecular-mass ASGPR subunits (HL-2), and binding and degradation of intact or desialylated Lp(a) were measured. In hedgehogs, one of the few species that synthesize Lp(a), most of the Lp(a) was taken up by the liver, followed by kidney and spleen. Lp(a) and asialo-Lp(a) were catabolized with apparent half-lives of 13.8 and 0.55 h respectively. Asialo-orosomucoide increased both half-lives significantly. In mice, the apparent half-life of Lp(a) was 4-6 h. Catabolism of native Lp(a) by wild-type mice was significantly faster compared with ASGPR- mice and there was a significantly greater accumulation of Lp(a) in the liver of ASGPR+ mice compared with ASGPR- mice. The catabolism of asialo-Lp(a) in ASGPR- mice was 8-fold faster when compared with native Lp(a) in wild-type mice. Transfected COS-7 cells expressing functional ASGPR showed approx. 5-fold greater binding and 2-fold faster degradation of native Lp(a) compared with control cells. Our results for the first time demonstrate a physiological function of ASGPR in the catabolism of Lp(a).
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Registered trials
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