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Lp(a) catabolism in hypercholesterolaemic individuals
Abstract
Three pieces of evidence are presented that suggest that LDL receptors are not greatly involved in the catabolism of intact Lp(a) in vivo. First, studies of normal and heterozygous familial hypercholesterolaemic (FH) siblings who have inherited identical apo(a) alleles have shown that the absence of effective LDL receptors is not invariably associated with an increase in the plasma concentration of Lp(a). Furthermore, in vitro competition studies with reduced Lp(a) from familial-defective apoB subjects indicate that their Lp(a), unlike their LDL, is not enriched with particles containing the binding-defective apoB. Finally, turnover studies in vivo showed no difference in catabolic rate for Lp(a) between normal and FH subjects. There was, however, evidence to suggest that LDL receptors could play a part in the ultimate clearance of Lp(a) by mediating the degradation of its lipid and apoB components after the removal of apo(a) in the circulation.
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Other studies in humans did not find a defect in Lp(a) catabolism for patients with Familial Hypercholesterolemia.
“other studies did not37-39.”
From Functional interrogation of cellular Lp(a) uptake by genome-scale CRISPR screening (2025) · cites this paper as [39]
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Research works printed but not linked: 8
- Armstrong, 1985, Isolation, characterization, and uptake in human fibroblasts of an apo(a)-free lipoprotein obtained on reduction of lipoprotein(a), J. Lipid Res., 26, 1314, 10.1016/S0022-2275(20)34257-7 · DOI
- Hofman, 1990, Overexpression of human low density lipoprotein receptors leads to accelerated catabolism of Lp(a) lipoprotein in transgenic mice, J. Clin. Invest., 85, 1542, 10.1172/JCI114602 · DOI · Paper page
- Innerarity, 1990, Familial defective apolipoprotein B-100: a mutation of apolipoprotein B that causes hypercholesterolemia, J. Lipid Res., 31, 1337, 10.1016/S0022-2275(20)42605-7 · DOI · Paper page
- Knight, 1991, Catabolism of lipoprotein(a) in familial hypercholesterolaemic subjects, Atherosclerosis, 87, 227, 10.1016/0021-9150(91)90025-X · DOI · Paper page
- Krempler, 1980, Turnover of lipoprotein(a) in man, J. Clin. Invest., 65, 1483, 10.1172/JCI109813 · DOI
- Perombelon, 1992, Lipoprotein(a) in subjects with familial defective apolipoprotein B100, Atherosclerosis, 92, 203, 10.1016/0021-9150(92)90279-P · DOI
- Soutar, 1991, Relationship between apolipoprotein(a) phenotype, lipoprotein(a) concentration in plasma, and low density lipoprotein receptor function in a large kindred with familial hypercholesterolemia due to the pro664 → leu mutation in the LDL receptor gene, J. Clin. Invest., 88, 483, 10.1172/JCI115329 · DOI
- Thiery, 1988, Serum lipoprotein Lp(a) concentrations are not influenced by an HMG CoA reductase inhibitor, Klin. Wochenschr., 66, 462, 10.1007/BF01745519 · DOI
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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
- Knight, B. L.
- Venue
- Chemistry and Physics of Lipids
- Publisher
- Elsevier BV
- Published
- 1994-01
- Volume
- 67-68
- Pages
- 233-239
- ISSN
- 0009-3084
- Cited by
- 17
- References
- 0
- Language
- en
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