ArticleJournal of lipid research2014
PCSK9 inhibition fails to alter hepatic LDLR, circulating cholesterol, and atherosclerosis in the absence of ApoE.
Article in Journal of lipid research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 81 citations in OpenAlex.
- PROTAC-mediated PCSK9 degradation attenuates atherosclerosis and improves plaque composition via suppression of NF-κB/TNF-α pathway.BMC medicine · 2026Article
- Obicetrapib and ezetimibe enhance LDL receptor-mediated VLDL clearance and regress atherosclerosis on atorvastatin background.Journal of lipid research · 2026Article
- Alirocumab Attenuated Plaque Inflammation and PCSK9-Induced Proinflammatory Signalling in M1 Macrophages Independently of Lipid Lowering.Biomolecules · 2026Article
- PCSK9 and coronary atherosclerosis progression beyond LDL-cholesterol in coronary artery disease patients.European journal of clinical investigation · 2025Article
- The designer cytokine IC7Fc attenuates atherosclerosis development by targeting hyperlipidemia in mice.Science advances · 2025Article
- LDL-Bound PCSK9 Has a Slower Clearance Kinetic and Higher Use for HSPGs Than Free-PCSK9-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Shared genetics of lung cancer and type 2 diabetes: a large-scale genome-wide cross-trait analysis.Translational lung cancer research · 2025Article
- Effects of life-long hyperlipidaemia on age-dependent development of endothelial dysfunction in humanised dyslipidaemic mice.GeroScience · 2025Article
- Silencing hepatic PCSK9 via novel chimeric AAV8 mitigates the progression of atherosclerosis by inhibiting inflammation in ApoEMolecular therapy. Methods & clinical development · 2025Article
- PCSK9 with a gain of function D374Y mutation aggravates atherosclerosis by inhibiting PPARα expression.Scientific reports · 2025Article
- Engineered extracellular vesicles as nanosponges for lysosomal degradation of PCSK9.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Polymorphisms in the proprotein convertase subtilisin/kexin type 9 gene in clinically diagnosed patients with familial hypercholesterolemia.Revista da Associacao Medica Brasileira (1992) · 2025Observational
- The Effects of Anti-thyroid Drugs on Lipoproteins and Insulin Resistance in Graves' Disease: A Randomized Clinical Trial.Journal of lipid and atherosclerosis · 2024Article
- Association between Apo B, LDL-R and PCSK9 gene polymorphisms with coronary artery diseases in Egyptians.Molecular biology reports · 2024Article
- Low or oscillatory shear stress and endothelial permeability in atherosclerosis.Frontiers in physiology · 2024Review
- Atherosclerosis: an overview of mouse models and a detailed methodology to quantify lesions in the aortic root.Vascular biology (Bristol, England) · 2024Review
- Pyrroloquinoline quinone inhibits PCSK9-NLRP3 mediated pyroptosis of Leydig cells in obese mice.Cell death & disease · 2023Article
- Involvement of APOE in Incidence of Revascularization in Patients Affected by Peripheral Arterial Disease: A Prospective Study from Southern Italy.Journal of clinical medicine · 2023Article
- Genetic or therapeutic neutralization of ALK1 reduces LDL transcytosis and atherosclerosis in mice.Nature cardiovascular research · 2023Article
- Atorvastatin Attenuates Diet-Induced Non-Alcoholic Steatohepatitis in APOE*3-Leiden Mice by Reducing Hepatic Inflammation.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LDL cholesterol (LDL-C) contributes to coronary heart disease. Proprotein convertase subtilisin/kexin type 9 (PCSK9) increases LDL-C by inhibiting LDL-C clearance. The therapeutic potential for PCSK9 inhibitors is highlighted by the fact that PCSK9 loss-of-function carriers exhibit 15-30% lower circulating LDL-C and a disproportionately lower risk (47-88%) of experiencing a cardiovascular event. Here, we utilized pcsk9(-/-) mice and an anti-PCSK9 antibody to study the role of the LDL receptor (LDLR) and ApoE in PCSK9-mediated regulation of plasma cholesterol and atherosclerotic lesion development. We found that circulating cholesterol and atherosclerotic lesions were minimally modified in pcsk9(-/-) mice on either an LDLR- or ApoE-deficient background. Acute administration of an anti-PCSK9 antibody did not reduce circulating cholesterol in an ApoE-deficient background, but did reduce circulating cholesterol (-45%) and TGs (-36%) in APOE*3Leiden.cholesteryl ester transfer protein (CETP) mice, which contain mouse ApoE, human mutant APOE3*Leiden, and a functional LDLR. Chronic anti-PCSK9 antibody treatment in APOE*3Leiden.CETP mice resulted in a significant reduction in atherosclerotic lesion area (-91%) and reduced lesion complexity. Taken together, these results indicate that both LDLR and ApoE are required for PCSK9 inhibitor-mediated reductions in atherosclerosis, as both are needed to increase hepatic LDLR expression.
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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.