The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
Galactose-specific asialoglycoprotein receptor is involved in lipoprotein (a) catabolism
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).
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Steady state levels of circulating Lp(a) depend on its rate of clearance, which occurs primarily in the liver.
“The steady state level of circulating Lp(a) also depends on its rate of clearance, which occurs primarily in the liver25,26.”
From Functional interrogation of cellular Lp(a) uptake by genome-scale CRISPR screening (2025) · cites this paper as [26]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
cDNA sequence of human apolipoprotein(a) is homologous to plasminogen
McLean, J. W., Tomlinson, J. E., Kuang, W.-J., Eaton, D. L., Chen, E. Y., Fless, G. M., Scanu, A. M., & Lawn, R. M. (1987) · Nature · doi:10.1038/330132a0 · Cited by 1,886 · cited 1×
“Apo(a) is a high-molecular-mass glycoprotein with repetitive domains, the so-called kringles (K), which show a high degree of sequence identity with plasminogen K-IV (kringle-4) [ 6 ].”
Background
Flagged first, then by citations
Research works printed but not linked: 1
- 18 Wo, X., Kostner, K., Frank, S. and Kostner, G. M. (1997) Assembly and catabolism of lipoprotein(a). In Proceedings of the 11th International Symposium on Atherosclerosis, Paris, 5-9 October 1997 (Jacotot, B., Mathe, D. and Fruchart, J.-C., eds.), pp. 567-574
Cited by
Sorted by citations
Hypomorphic ASGR1 modulates lipid homeostasis via INSIG1-mediated SREBP signaling suppression
Xu, Y., Tao, J., Yu, X., Wu, Y., Chen, Y., You, K., Zhang, J., Getachew, A., Pan, T., Zhuang, Y., et al. (2021) · JCI Insight · doi:10.1172/jci.insight.147038 · Cited by 45
Functional interrogation of cellular Lp(a) uptake by genome-scale CRISPR screening
Khan, T. G., Bragazzi Cunha, J., Raut, C., Burroughs, M., Vyas, H. S., Leix, K., Goonewardena, S. N., Smrcka, A. V., Speliotes, E. K., & Emmer, B. T. (2025) · Atherosclerosis · doi:10.1016/j.atherosclerosis.2025.119174 · Cited by 6
Metadata
- Authors
- HRZENJAK, A., FRANK, S., WO, X., ZHOU, Y., van BERKEL, T., & KOSTNER, G. M.
- Affiliations
- Institute of Medical Biochemistry and Medical Molecular Biology, University of Graz, Austria, Harrachgasse 21, A-8010 Graz, Austria
- Molecular Medical Institute, Zhejing Traditional Chinese Medical College, People's Republic of China
- Center for Bio-Pharmaceutical Sciences, Gorlaeus Laboratory, Leiden, The Netherlands
- Venue
- Biochemical Journal
- Publisher
- Portland Press Ltd.
- Published
- 2003-12-15
- Volume
- 376
- Issue
- 3
- Pages
- 765-771
- ISSN
- 0264-6021
- 1470-8728
- Cited by
- 51
- References
- 1
- Language
- en
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review