Evidence map›Paper›PMID 37730951›Full record

ArticleScientific reports2023

Generation of a familial hypercholesterolemia model in non-human primate.

Akira Sato, Tomoyuki Tsukiyama, Masahiro Komeno, Chizuru Iwatani, Hideaki Tsuchiya, Ikuo Kawamoto, Mitsuru Murase, Takahiro Nakagawa, Iori Itagaki, Yasunari Seita and 6 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 1 institution in 1 country.

Akira SatoDivision of Molecular Medical Biochemistry, Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Seta Tsukinowa-Cho, Otsu, Shiga, 520-2192, Japan.
Tomoyuki TsukiyamaResearch Center for Animal Life Science, Shiga University of Medical Science, Otsu, Japan.
Masahiro KomenoDivision of Molecular Medical Biochemistry, Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Seta Tsukinowa-Cho, Otsu, Shiga, 520-2192, Japan.
Chizuru IwataniResearch Center for Animal Life Science, Shiga University of Medical Science, Otsu, Japan.
Hideaki TsuchiyaResearch Center for Animal Life Science, Shiga University of Medical Science, Otsu, Japan.
Ikuo KawamotoResearch Center for Animal Life Science, Shiga University of Medical Science, Otsu, Japan.
Mitsuru MuraseResearch Center for Animal Life Science, Shiga University of Medical Science, Otsu, Japan.
Takahiro NakagawaResearch Center for Animal Life Science, Shiga University of Medical Science, Otsu, Japan.
Iori ItagakiResearch Center for Animal Life Science, Shiga University of Medical Science, Otsu, Japan.
Yasunari SeitaDepartment of Stem Cells and Human Disease Models, Research Center for Animal Life Science, Shiga University of Medical Science, Otsu, Japan.
Shoma MatsumotoDepartment of Stem Cells and Human Disease Models, Research Center for Animal Life Science, Shiga University of Medical Science, Otsu, Japan.
Masataka NakayaResearch Center for Animal Life Science, Shiga University of Medical Science, Otsu, Japan.
Akio ShimizuDivision of Molecular Medical Biochemistry, Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Seta Tsukinowa-Cho, Otsu, Shiga, 520-2192, Japan.
Atsushi YamadaMedical Innovation Research Center, Shiga University of Medical Science, Otsu, Japan.
Masatsugu EmaResearch Center for Animal Life Science, Shiga University of Medical Science, Otsu, Japan.
Hisakazu OgitaDivision of Molecular Medical Biochemistry, Department of Biochemistry and Molecular Biology, Shiga University of Medical Science, Seta Tsukinowa-Cho, Otsu, Shiga, 520-2192, Japan. hogita@belle.shiga-med.ac.jp.
Shiga University of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Familial hypercholesterolemia (FH) is an inherited autosomal dominant disorder that is associated with a high plasma level of low-density lipoprotein (LDL) cholesterol, leading to an increased risk of cardiovascular diseases. To develop basic and translational research on FH, we here generated an FH model in a non-human primate (cynomolgus monkeys) by deleting the LDL receptor (LDLR) gene using the genome editing technique. Six LDLR knockout (KO) monkeys were produced, all of which were confirmed to have mutations in the LDLR gene by sequence analysis. The levels of plasma cholesterol and triglyceride were quite high in the monkeys, and were similar to those in FH patients with homozygous mutations in the LDLR gene. In addition, periocular xanthoma was observed only 1 year after birth. Lipoprotein profile analysis showed that the plasma very low-density lipoprotein and LDL were elevated, while the plasma high density lipoprotein was decreased in LDLR KO monkeys. The LDLR KO monkeys were also strongly resistant to medications for hypercholesterolemia. Taken together, we successfully generated a non-human primate model of hypercholesterolemia in which the phenotype is similar to that of homozygous FH patients.

Indexed as

Craniocerebral TraumaHypercholesterolemiaHyperlipoproteinemia Type IIAnimalsHumansLipoproteins, LDLMacaca fascicularisPrimatesLipoproteins, LDL

Identifiers

PMID37730951
PMCPMC10511719
OpenAlexW4386886094

What Socratic holds

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Registered trials

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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 Socratic graph.