ArticleEBioMedicine2018
Spontaneous severe hypercholesterolemia and atherosclerosis lesions in rabbits with deficiency of low-density lipoprotein receptor (LDLR) on exon 7.
Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.
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Who cites it
33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 58 citations in OpenAlex.
- The promising novel therapies for familial hypercholesterolemia.Journal of clinical laboratory analysis · 2022Pooled it
- Preclinical techniques to investigate exercise training in vascular pathophysiology.American journal of physiology. Heart and circulatory physiology · 2021Pooled it
- Broad-spectrum host-targeting antivirals for rhinovirus infections: mechanisms and future perspectives.Frontiers in immunology · 2026Review
- Correlation Between Oral Bacteria and Atherosclerotic Thrombotic Disease: Advances in Animal Model Studies.Current atherosclerosis reports · 2025Review
- Deciphering the Enigma of Calcific Aortic Valve Disease: The Pivotal Role of Animal Models in Unraveling Pathogenesis and Advancing Therapeutic Strategies.Biomedicines · 2025Review
- Current status and challenges of multi-omics research using animal models of atherosclerosis.Journal of molecular and cellular cardiology plus · 2025Review
- Targeting Liver Epsins Ameliorates Dyslipidemia in Atherosclerosis through Inhibition of Proprotein Convertase Subtilisin/Kexin Type 9-Mediated Low-density Lipoprotein Receptor Degradation.bioRxiv : the preprint server for biology · 2025Article
- From Bench to Bedside: Translational Approaches to Cardiotoxicity in Breast Cancer, Lung Cancer, and Lymphoma Therapies.Cancers · 2025Review
- Cellular Phenotypic Transformation During Atherosclerosis: The Potential Role of miRNAs as Biomarkers.International journal of molecular sciences · 2025Review
- CRISPR/Cas System: A Powerful Strategy to Improve Monogenic Human Diseases as Therapeutic Delivery; Current Applications and Challenges.Current gene therapy · 2025Review
- Gene editing therapy as a therapeutic approach for cardiovascular diseases in animal models: A scoping review.PloS one · 2025Article
- Review
- Applications of Genome Editing Technologies in CAD Research and Therapy with a Focus on Atherosclerosis.International journal of molecular sciences · 2023Review
- Translating atherosclerosis research from bench to bedside: navigating the barriers for effective preclinical drug discovery.Clinical science (London, England : 1979) · 2022Article
- Delphinidin-3-Pharmaceutical biology · 2022Article
- Non-Mouse Models of Atherosclerosis: Approaches to Exploring the Translational Potential of New Therapies.International journal of molecular sciences · 2022Review
- Pathological Investigations of Intracranial Atherosclerosis Using Multiple Hypercholesterolemic Rabbit Models.Frontiers in endocrinology · 2022Article
- Preclinical models of radiation-induced cardiac toxicity: Potential mechanisms and biomarkers.Frontiers in oncology · 2022Review
- CRISPR/Cas9-mediated knockout of APOC3 stabilizes plasma lipids and inhibits atherosclerosis in rabbits.Lipids in health and disease · 2021Article
- Genetically-engineered hamster models: applications and perspective in dyslipidemia and atherosclerosis-related cardiovascular disease.Medical review (2021) · 2021Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Rabbits (Oryctolagus cuniculus) have been the very frequently used as animal models in the study of human lipid metabolism and atherosclerosis, because they have similar lipoprotein metabolism to humans. Most of hyperlipidemia and atherosclerosis rabbit models are produced by feeding rabbits a high-cholesterol diet. Gene editing or knockout (KO) offered another means of producing rabbit models for study of the metabolism of lipids and lipoproteins. Even so, apolipoprotein (Apo)E KO rabbits must be fed a high-cholesterol diet to induce hyperlipidemia. In this study, we used the CRISPR/Cas9 system anchored exon 7 of low-density lipoprotein receptor (LDLR) in an attempt to generate KO rabbits. We designed two sgRNA sequences located in E7:g.7055-7074 and E7:g.7102-7124 of rabbit LDLR gene, respectively. Seven LDLR-KO founder rabbits were generated, and all of them contained biallelic modifications. Various mutational LDLR amino acid sequences of the 7 founder rabbits were subjected to tertiary structure modeling with SWISS-MODEL, and results showed that the structure of EGF-A domain of each protein differs from the wild-type. All the founder rabbits spontaneously developed hypercholesterolemia and atherosclerosis on a normal chow (NC) diet. Analysis of their plasma lipids and lipoproteins at the age of 12 weeks revealed that all these KO rabbits exhibited markedly increased levels of plasma TC (the highest of which was 1013.15 mg/dl, 20-fold higher than wild-type rabbits), LDL-C (the highest of which was 730.00 mg/dl, 35-fold higher than wild-type rabbits) and TG accompanied by reduced HDL-C levels. Pathological examinations of a founder rabbit showed prominent aortic atherosclerosis lesions and coronary artery atherosclerosis.In conclusion, we have reported the generation LDLR-KO rabbit model for the study of spontaneous hypercholesterolemia and atherosclerosis on a NC diet. The LDLR-KO rabbits should be a useful rabbit model of human familial hypercholesterolemia (FH) for the simulations of human primary hypercholesterolemia and such models would allow more exact research into cardio-cerebrovascular disease.
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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.