ArticleLipids in health and disease2021
CRISPR/Cas9-mediated knockout of APOC3 stabilizes plasma lipids and inhibits atherosclerosis in rabbits.
Article in Lipids in health and disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- Inherited risk of coronary artery disease: redefining care with imaging and genetics.Nature reviews. Cardiology · 2026Review
- Beneficial Changes in Apolipoprotein Concentrations After Bariatric Surgery in Obese Women.Metabolites · 2026Article
- Atherogenic apolipoprotein C-III may not be as bad as we thought.Journal of thrombosis and haemostasis : JTH · 2026Article
- Review
- Olezarsen and Beyond: Emerging Targeted Treatments for Familial Chylomicronemia Syndrome and Related Triglyceride Disorders.Journal of lipid and atherosclerosis · 2026Review
- TGF-β: The Molecular Mechanisms of Atherosclerosis - insights into SMAD Pathways and Gene Therapy Prospects.Current medicinal chemistry · 2026Review
- Apolipoprotein C3 Promotes Angiogenesis in an Inflammatory Mouse Model of Peripheral Artery Disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Hypertriglyceridemia as a Key Contributor to Abdominal Aortic Aneurysm Development and Rupture: Insights From Genetic and Experimental Models.Circulation · 2025Article
- Gene Therapy Approaches for Atherosclerosis Focusing on Targeting Lipid Metabolism and Inflammation.International journal of molecular sciences · 2025Review
- Novel Therapeutics for Familial Chylomicronemia Syndrome.Current atherosclerosis reports · 2025Review
- Associations Between APOC3 and ANGPTL8 Gene Polymorphisms With MASLD Risk and the Mediation Effect of Triglyceride on MASLD in the Chinese Population.Journal of cellular and molecular medicine · 2025Article
- Remnant cholesterol concentrations best explain the cardiovascular benefit of APOC3 genetic inhibition: a drug target Mendelian randomization study.European heart journal open · 2025Article
- Review
- Endothelial Dysfunction in Atherosclerosis: Experimental Models and Therapeutics.Biomaterials research · 2025Review
- Gene editing therapy as a therapeutic approach for cardiovascular diseases in animal models: A scoping review.PloS one · 2025Article
- Multifaceted Role of Apolipoprotein C3 in Cardiovascular Disease Risk and Metabolic Disorder in Diabetes.International journal of molecular sciences · 2024Review
- Emerging Trends and Innovations in the Treatment and Diagnosis of Atherosclerosis and Cardiovascular Disease: A Comprehensive Review towards Healthier Aging.Pharmaceutics · 2024Review
- Therapeutic Gene Editing in Dyslipidemias.Reviews in cardiovascular medicine · 2024Review
- A novel mouse model of familial combined hyperlipidemia and atherosclerosis.Acta pharmacologica Sinica · 2024Article
- Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundHigh levels of apolipoprotein C3 (APOC3) can lead to hypertriglyceridemia, which increases the risk of cardiovascular disease. We aim to create APOC3-knockout (KO) rabbits and explore the effects of APOC3 deletion on the occurrence and development of atherosclerosis.
methodsAn sgRNA anchored to exon 2 of APOC3 was designed to edit embryo genomes using the CRISPR/Cas9 system. The founder rabbits were sequenced, and their lipid profile, inflammatory cytokines, and atherosclerotic plaques were analyzed.
resultsWhen given a normal chow (NC) diet, all APOC3-KO rabbits had 50% lower triglyceride (TG) levels than those of the matched age control group. Additionally, their plasma lipoprotein lipase increased. When fed a high-fat diet, APOC3 deficiency was observed to be more conducive to the maintenance of plasma TG, total cholesterol, and low-density lipoprotein cholesterol levels, and the inhibition of the inflammatory response and the protection against atherosclerosis in rabbits.
conclusionAPOC3 deficiency can delay the formation of atherosclerosis-induced HFD in rabbits, indicating this is a novel therapeutic target to treat atherosclerosis.
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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.