ArticleGenetics2006
Quantitative trait locus analysis of atherosclerosis in an intercross between C57BL/6 and C3H mice carrying the mutant apolipoprotein E gene.
Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
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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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Who cites it
38 citing papers in PubMed, 48 citations in OpenAlex.
- Mouse Models of Atherosclerosis: What They Teach Us, What They Miss, and When to Use Them.Bioengineering (Basel, Switzerland) · 2026Review
- Cholesterol metabolism: molecular mechanisms, biological functions, diseases, and therapeutic targets.Molecular biomedicine · 2025Review
- Article
- Regional Variation in Genetic Control of Atherosclerosis in Hyperlipidemic Mice.G3 (Bethesda, Md.) · 2020Article
- Data on genetic linkage of oxidative stress with cardiometabolic traits in an intercross derived from hyperlipidemic mouse strains.Data in brief · 2020Article
- Genetic linkage of oxidative stress with cardiometabolic traits in an intercross derived from hyperlipidemic mouse strains.Atherosclerosis · 2020Article
- Loss of reticulocalbin 2 lowers blood pressure and restrains ANG II-induced hypertension in vivo.American journal of physiology. Renal physiology · 2019Article
- Atherogenesis in the Carotid Artery with and without Interrupted Blood Flow of Two Hyperlipidemic Mouse Strains.Journal of vascular research · 2019Article
- ApoE facilitates the microglial response to amyloid plaque pathology.The Journal of experimental medicine · 2018Article
- Article
- Genetic analysis of a mouse cross implicates an anti-inflammatory gene in control of atherosclerosis susceptibility.Mammalian genome : official journal of the International Mammalian Genome Society · 2017Article
- Genetic analysis of atherosclerosis identifies a major susceptibility locus in the major histocompatibility complex of mice.Atherosclerosis · 2016Article
- Mapping and Congenic Dissection of Genetic Loci Contributing to Hyperglycemia and Dyslipidemia in Mice.PloS one · 2016Article
- Genetic Architecture of Atherosclerosis in Mice: A Systems Genetics Analysis of Common Inbred Strains.PLoS genetics · 2015Article
- Genetic linkage of hyperglycemia and dyslipidemia in an intercross between BALB/cJ and SM/J Apoe-deficient mouse strains.BMC genetics · 2015Article
- Influence of phthalates on glucose homeostasis and atherosclerosis in hyperlipidemic mice.BMC endocrine disorders · 2015Article
- PET imaging detection of macrophages with a formyl peptide receptor antagonist.Nuclear medicine and biology · 2015Article
- Variation in Type 2 Diabetes-Related Phenotypes among Apolipoprotein E-Deficient Mouse Strains.PloS one · 2015Article
- Effect of the Kv1.3 voltage-gated potassium channel blocker PAP-1 on the initiation and progress of atherosclerosis in a rat model.Heart and vessels · 2015Article
- A mutation in Ampd2 is associated with nephrotic syndrome and hypercholesterolemia in mice.Lipids in health and disease · 2014Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Inbred mouse strains C57BL/6J (B6) and C3H/HeJ (C3H) differ significantly in atherosclerosis susceptibility and plasma lipid levels on the apolipoprotein E-deficient (apoE-/-) background when fed a Western diet. To determine genetic factors contributing to the variations in these phenotypes, we performed quantitative trait locus (QTL) analysis using an intercross between the two strains carrying the apoE-/- gene. Atherosclerotic lesions at the aortic root and plasma lipid levels of 234 female F2 mice were analyzed after being fed a Western diet for 12 weeks. QTL analysis revealed one significant QTL, named Ath22 (42 cM, LOD 4.1), on chromosome 9 and a suggestive QTL near D11mit236 (20 cM, LOD 2.4) on chromosome 11 that influenced atherosclerotic lesion size. One significant QTL on distal chromosome 1, which accounted for major variations in plasma LDL/VLDL cholesterol and triglyceride levels, coincided with a QTL having strong effects on body weight. Plasma LDL/VLDL cholesterol or triglyceride levels of F2 mice were significantly correlated with body weight, but they were not correlated with atherosclerotic lesion sizes. These data indicate that atherosclerosis susceptibility and plasma cholesterol levels are controlled by separate genetic factors in the B6 and C3H mouse model and that genetic linkages exist between body weight and lipoprotein metabolism.
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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.