Evidence map›Paper›PMID 29289533›Full record

ArticleEBioMedicine2018

LDL Receptor Gene-ablated Hamsters: A Rodent Model of Familial Hypercholesterolemia With Dominant Inheritance and Diet-induced Coronary Atherosclerosis.

Xin Guo, Mingming Gao, Yunan Wang, Xiao Lin, Liu Yang, Nathan Cong, Xiangbo An, Feng Wang, Kai Qu, Liqing Yu and 5 more

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
7.4field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.

  1. Pooled it
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 2 countries.

Xin GuoInstitute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University, Beijing 100191, China.
Mingming GaoLipid Metabolism Laboratory, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang, China.
Yunan WangInstitute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University, Beijing 100191, China.
Xiao LinInstitute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University, Beijing 100191, China.
Liu YangState Key Laboratory of Bioactive Substance, Function of Natural Medicines & Ministry of Health Key Laboratory of Biosynthesis of Natural Products, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Nathan CongInstitute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University, Beijing 100191, China.
Xiangbo AnDepartment of Interventional Radiology, First Affiliated Hospital of Dalian Medical University, Dalian 110611, China.
Feng WangDepartment of Interventional Radiology, First Affiliated Hospital of Dalian Medical University, Dalian 110611, China.
Kai QuState Key Laboratory of Bioactive Substance, Function of Natural Medicines & Ministry of Health Key Laboratory of Biosynthesis of Natural Products, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Liqing YuCenter for Molecular and Translational Medicine, Institute for Biomedical Sciences, Georgia State University, Atlanta, GA 30303, USA.
Yuhui WangInstitute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University, Beijing 100191, China.
Jinjie WangInstitute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University, Beijing 100191, China.
Haibo ZhuState Key Laboratory of Bioactive Substance, Function of Natural Medicines & Ministry of Health Key Laboratory of Biosynthesis of Natural Products, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Xunde XianDepartment of Molecular Genetics, UT Southwestern Medical Center, Dallas, TX 75390, USA; Department of Biochemistry and Molecular Biology, College of Basic Medicine, Hebei Medical University, Shijiazhuang, China. Electronic address: xunde.xian@utsouthwestern.edu.
George LiuInstitute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University, Beijing 100191, China. Electronic address: georgeliu@bjmu.edu.cn.
Peking University · CNChinese Academy of Medical Sciences & Peking Union Medical College · CNFirst Affiliated Hospital of Dalian Medical University · CNHebei Medical University · CNGeorgia State University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Familial hypercholesterolemia (FH) is an autosomal dominant genetic disease caused mainly by LDL receptor (Ldlr) gene mutations. Unlike FH patients, heterozygous Ldlr knockout (KO) mice do not show a dominant FH trait. Hamsters, like humans, have the cholesteryl ester transfer protein, intestine-only ApoB editing and low hepatic cholesterol synthesis. Here, we generated Ldlr-ablated hamsters using CRISPR/Cas9 technology. Homozygous Ldlr KO hamsters on a chow diet developed hypercholesterolemia with LDL as the dominant lipoprotein and spontaneous atherosclerosis. On a high-cholesterol/high-fat (HCHF) diet, these animals exhibited severe hyperlipidemia and atherosclerotic lesions in the aorta and coronary arteries. Moreover, the heterozygous Ldlr KO hamsters on a short-term HCHF diet also had overt hypercholesterolemia, which could be effectively ameliorated with several lipid-lowering drugs. Importantly, heterozygotes on 3-month HCHF diets developed accelerated lesions in the aortas and coronary arteries. Our findings demonstrate that the Ldlr KO hamster is an animal model of choice for human FH and has great potential in translational research of hyperlipidemia and coronary heart disease.

Indexed as

Genes, DominantAnimalsAortaAtherosclerosisBase SequenceCoronary VesselsCricetinaeCRISPR-Cas SystemsDisease Models, AnimalGene Knockout TechniquesHumansHyperlipoproteinemia Type IIInheritance PatternsLipidsLipoproteinsMaleLipidsLipoproteinsReceptors, LDLAtherosclerosisCRISPR/Cas9Golden Syrian hamsterHyperlipidemiaLDL receptor

Identifiers

PMID29289533
PMCPMC5828369
OpenAlexW2773721653

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.