ArticleCirculation research2013
Loss of plasma proprotein convertase subtilisin/kexin 9 (PCSK9) after lipoprotein apheresis.
Article in Circulation research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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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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.
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Who cites it
28 citing papers in PubMed.
- Trial
- LDL-Bound PCSK9 Has a Slower Clearance Kinetic and Higher Use for HSPGs Than Free-PCSK9-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Low-density lipoprotein cholesterol levels and in-hospital bleeding in patients with atrial fibrillation: findings from CCC-AF project.Frontiers in cardiovascular medicine · 2025Article
- Soluble endoglin as a biomarker of successful rheopheresis treatment in patients with age-related macular degeneration.Scientific reports · 2024Article
- Lipoprotein Apheresis: Current Recommendations for Treating Familial Hypercholesterolemia and Elevated Lipoprotein(a).Current atherosclerosis reports · 2023Review
- Proteomics and Lipidomics to unveil the contribution of PCSK9 beyond cholesterol lowering: a narrative review.Frontiers in cardiovascular medicine · 2023Review
- The Role of Endothelial Progenitor Cells in Atherosclerosis and Impact of Anti-Lipemic Treatments on Endothelial Repair.International journal of molecular sciences · 2022Review
- Pathogenic gain-of-function mutations in the prodomain and C-terminal domain of PCSK9 inhibit LDL binding.Frontiers in physiology · 2022Article
- The Association of Proprotein Convertase Subtilisin/Kexin Type 9 to Plasma Low-Density Lipoproteins: An Evaluation of Different Methods.Metabolites · 2021Article
- Familial Hypercholesterolemia and Lipoprotein Apheresis.Journal of atherosclerosis and thrombosis · 2019Review
- Cell-associated heparin-like molecules modulate the ability of LDL to regulate PCSK9 uptake.Journal of lipid research · 2019Article
- Proprotein Convertase Subtilisin/Kexin Type 9, Brain Cholesterol Homeostasis and Potential Implication for Alzheimer's Disease.Frontiers in aging neuroscience · 2019Article
- PCSK9: From Basic Science Discoveries to Clinical Trials.Circulation research · 2018Review
- NHLBI Working Group Recommendations to Reduce Lipoprotein(a)-Mediated Risk of Cardiovascular Disease and Aortic Stenosis.Journal of the American College of Cardiology · 2018Review
- Threshold Effects of Circulating Angiopoietin-Like 3 Levels on Plasma Lipoproteins.The Journal of clinical endocrinology and metabolism · 2017Article
- PCSK9 and Atherosclerosis - Lipids and Beyond.Journal of atherosclerosis and thrombosis · 2017Review
- Clinical utility of evolocumab in the management of hyperlipidemia: patient selection and follow-up.Drug design, development and therapy · 2017Review
- PCSK9 Modulates the Secretion But Not the Cellular Uptake of Lipoprotein(a) Ex Vivo: An Effect Blunted by Alirocumab.JACC. Basic to translational science · 2016Article
- Biology of proprotein convertase subtilisin kexin 9: beyond low-density lipoprotein cholesterol lowering.Cardiovascular research · 2016Review
- PCSK9 inhibitors in the prevention of cardiovascular disease.Journal of thrombosis and thrombolysis · 2016Review
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Authors and funding
4 authors.
Funding
Abstract
rationaleLipoprotein apheresis (LA) reduces low-density lipoprotein (LDL) levels in patients with severe familial hypercholesterolemia (FH). We have recently reported that >30% of plasma proprotein convertase subtilisin/kexin 9 (PCSK9) is bound to LDL, thus we predicted that LA would also reduce plasma PCSK9 levels by removing LDL.
objectivePre- and post-apheresis plasma from 6 patients with familial hypercholesterolemia on 3 consecutive treatment cycles was used to determine changes in PCSK9 levels. METHODS AND
resultsLA drastically reduced plasma LDL (by 77 ± 4%). Concomitantly, PCSK9 levels fell by 52 ± 5%, strongly correlating with the LDL drop (P=0.0322; r(2)=0.26), but not with decreases in triglyceride (49 ± 13%) or high-density lipoprotein levels (18 ± 2%). Levels of albumin, creatinine, and CK-MB did not show significant changes after LA. Similar to LDL, PCSK9 levels returned to pretreatment values between cycles (2-week intervals). Fractionation of pre- and post-apheresis plasma showed that 81 ± 11% of LDL-bound PCSK9 and 48 ± 14% of apolipoprotein B-free PCSK9 were removed. Separation of whole plasma, purified LDL, or the apolipoprotein B-free fraction through a scaled-down, experimental dextran sulfate cellulose beads column produced similar results.
conclusionsOur results show, for the first time, that modulation of LDL levels by LA directly affects plasma PCSK9 levels, and suggest that PCSK9 reduction is an additional benefit of LA. Because the loss of PCSK9 could contribute to the LDL-lowering effect of LA, then (1) anti-PCSK9 therapies may reduce frequency of LA in patients currently approved for therapy, and (2) LA and anti-PCSK9 therapies may be used synergistically to reduce treatment burden.
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