ArticleThe Journal of clinical investigation1995
Atherogenesis in transgenic mice with human apolipoprotein B and lipoprotein (a).
Article in The Journal of clinical investigation, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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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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.
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Who cites it
21 citing papers in PubMed, 94 citations in OpenAlex.
- Mouse Models of Atherosclerosis: What They Teach Us, What They Miss, and When to Use Them.Bioengineering (Basel, Switzerland) · 2026Review
- Cerebrovascular Changes and Neurodegeneration Related to Hyperlipidemia: Characteristics of the Human ApoB-100 Transgenic Mice.Current pharmaceutical design · 2020Article
- Proteomic Analysis of Liver from Human Lipoprotein(a) Transgenic Mice Shows an Oxidative Stress and Lipid Export Response.BioMed research international · 2018Article
- Development of lipoprotein(a) siRNAs for mechanism of action studies in non-human primate models of atherosclerosis.Journal of cardiovascular translational research · 2015Article
- Mouse models of atherosclerosis: explaining critical roles of lipid metabolism and inflammation.Journal of applied genetics · 2013Review
- Inhibition of neointima formation through DNA vaccination for apolipoprotein(a): a new therapeutic strategy for lipoprotein(a).Scientific reports · 2013Article
- Article
- Farnesoid X receptor represses hepatic human APOA gene expression.The Journal of clinical investigation · 2011Article
- Lipoprotein(a): an elusive cardiovascular risk factor.Arteriosclerosis, thrombosis, and vascular biology · 2004Review
- Lipoprotein(a): biology and clinical importance.The Clinical biochemist. Reviews · 2004Article
- Adenovirus-mediated apo(a)-antisense-RNA expression efficiently inhibits apo(a) synthesis in vitro and in vivo.Gene therapy · 2001Article
- MCP-1 deficiency reduces susceptibility to atherosclerosis in mice that overexpress human apolipoprotein B.The Journal of clinical investigation · 1999Article
- Review
- Low density lipoprotein receptor-negative mice expressing human apolipoprotein B-100 develop complex atherosclerotic lesions on a chow diet: no accentuation by apolipoprotein(a).Proceedings of the National Academy of Sciences of the United States of America · 1998Article
- Lipoprotein(a) vascular accumulation in mice. In vivo analysis of the role of lysine binding sites using recombinant adenovirus.The Journal of clinical investigation · 1997Article
- Modification of apolipoprotein(a) lysine binding site reduces atherosclerosis in transgenic mice.The Journal of clinical investigation · 1997Article
- Susceptibility to atherosclerosis in mice expressing exclusively apolipoprotein B48 or apolipoprotein B100.The Journal of clinical investigation · 1997Article
- Paradoxical enhancement of atherosclerosis by probucol treatment in apolipoprotein E-deficient mice.The Journal of clinical investigation · 1997Article
- Kringle-containing fragments of apolipoprotein(a) circulate in human plasma and are excreted into the urine.The Journal of clinical investigation · 1996Article
- Inhibition of atherosclerosis in CD4 T-cell-ablated and nude (nu/nu) C57BL/6 hyperlipidemic mice.The American journal of pathology · 1996Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The engineering of mice that express a human apoB transgene has resulted in animals with high levels of human-like LDL particles and through crosses with human apo(a) transgenics, high levels of human-like lipoprotein (a) (Lp[a]) particles. In this study, these animals have been used to compare the atherogenic properties of apo(a), LDL, and Lp(a). The presence of the high expressing apoB (apoBH) transgene was associated with a 2.5-fold increase in VLDL-LDL cholesterol (primarily in the LDL fraction) and a 15-fold increase in proximal lesions compared with non-transgenic mice (P < or = 0.0001), while the presence of the low expressing human apoB (apoBL) transgene was not associated with major changes in lipoprotein profiles or increases in aortic lesion size. Examination of aortas of apoBH mice demonstrated lesions along the entire length of the aorta and immunochemical analysis of the lesions revealed features characteristically seen in human lesions including the presence of oxidized lipoproteins, macrophages, and immunoglobulins. Unlike animals with the apoBL transgene, animals with the apo(a) transgene had significant increases in proximal aortic fatty streak lesions compared to nontransgenic control animals (threefold; P < 0.02), while animals with both transgenes, the apo(a)/apo BL double transgenics, had lesions 2.5 times greater than animals expressing the apo(a) transgene alone and eightfold (P < 0.0006) greater than nontransgenic animals. These murine studies demonstrate that marked increases in apoB and LDL resulted in atherosclerotic lesions extending down the aorta which resemble human lesions immunochemically and suggest that apo(a) associated with apoB and lipid may result in a more pro-atherogenic state than when apo(a) is free in plasma.
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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.