Evidence map›Paper›PMID 32757647›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2020

Apolipoprotein CIII Deficiency Protects Against Atherosclerosis in Knockout Rabbits.

Haizhao Yan, Manabu Niimi, Fumikazu Matsuhisa, Huanjin Zhou, Shuji Kitajima, Yajie Chen, Chuan Wang, Xiawen Yang, Jian Yao, Dongshan Yang and 8 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

22 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Atherogenic apolipoprotein C-III may not be as bad as we thought.Journal of thrombosis and haemostasis : JTH · 2026
    Article
  3. Review
  4. Review
  5. Review
  6. Molecular Regulation and Therapeutic Targeting of VLDL Production in Cardiometabolic Disease.Cellular and molecular gastroenterology and hepatology · 2025
    Review
  7. Review
  8. Review
  9. Review
  10. Apolipoprotein C3: form begets function.Journal of lipid research · 2024
    Review
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
  16. Is apoCIII-Lowering A Double-Edged Sword?Journal of atherosclerosis and thrombosis · 2022
    Article
  17. Gene editing and its applications in biomedicine.Science China. Life sciences · 2022
    Review
  18. A Tale of Two New Targets for Hypertriglyceridaemia: Which Choice of Therapy?BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2022
    Review
  19. Article
  20. 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

18 authors at 8 institutions in 3 countries.

Haizhao Yan *From the Department of Molecular Pathology, Faculty of Medicine, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Japan (H.Y., M.N., H.Z., Y.C., C.W., J.F.).
Manabu Niimi *From the Department of Molecular Pathology, Faculty of Medicine, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Japan (H.Y., M.N., H.Z., Y.C., C.W., J.F.).
Fumikazu Matsuhisa *Division of Biological Science and Development, Analytical Research Center for Experimental Sciences, Saga University, Japan (F.M., S.K.).
Huanjin ZhouFrom the Department of Molecular Pathology, Faculty of Medicine, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Japan (H.Y., M.N., H.Z., Y.C., C.W., J.F.).
Shuji KitajimaDivision of Biological Science and Development, Analytical Research Center for Experimental Sciences, Saga University, Japan (F.M., S.K.).
Yajie ChenFrom the Department of Molecular Pathology, Faculty of Medicine, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Japan (H.Y., M.N., H.Z., Y.C., C.W., J.F.).
Chuan WangFrom the Department of Molecular Pathology, Faculty of Medicine, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Japan (H.Y., M.N., H.Z., Y.C., C.W., J.F.).
Xiawen YangDivision of Molecular Signaling, Department of the Advanced Biomedical Research, Faculty of Medicine, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Japan (X.Y., J.Y.).
Jian YaoDivision of Molecular Signaling, Department of the Advanced Biomedical Research, Faculty of Medicine, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Japan (X.Y., J.Y.).
Dongshan YangCenter for Advanced Models for Translational Sciences and Therapeutics, University of Michigan Medical Center, Ann Arbor (D.Y., J.Z., Y.E.C.).
Jifeng ZhangCenter for Advanced Models for Translational Sciences and Therapeutics, University of Michigan Medical Center, Ann Arbor (D.Y., J.Z., Y.E.C.).
Masami MurakamiDepartment of Clinical Laboratory Medicine, Gunma University, Graduate School of Medicine, Maebashi, Japan (M.M., K.N.).
Katsuyuki NakajimaDepartment of Clinical Laboratory Medicine, Gunma University, Graduate School of Medicine, Maebashi, Japan (M.M., K.N.).
Yao WangSchool of Biotechnology and Health Sciences, Wuyi University, Jiangmen, China (Y.W., J.F.).
Enqi LiuResearch Institute of Atherosclerotic Disease and Laboratory Animal Center, Xi'an Jiaotong University School of Medicine, China (E.L.).
Jingyan LiangInstitute of Translational Medicine, Medical College, Yangzhou University, China (J.L.).
Y Eugene ChenCenter for Advanced Models for Translational Sciences and Therapeutics, University of Michigan Medical Center, Ann Arbor (D.Y., J.Z., Y.E.C.).
Jianglin FanFrom the Department of Molecular Pathology, Faculty of Medicine, Interdisciplinary Graduate School of Medicine, University of Yamanashi, Chuo, Japan (H.Y., M.N., H.Z., Y.C., C.W., J.F.).
University of Yamanashi · JPUniversity of Michigan · USGunma University · JPSaga University · JPWuyi University · CNGuangzhou Institutes of Biomedicine and Health · CNXi'an Jiaotong University · CNYangzhou University · CN

Funding

IDOL and dyslipidemia in cardiovascular diseasesR01HL147527 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2019 to 2022
$3.1M
MPO, HDL Dysfunction and Cardiovascular DiseaseR01HL129778 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2015 to 2018
$2.9M
CETP and HDL Function in Cardiovascular DiseasesR01HL117491 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2013 to 2016
$2.4M
NHLBI NIH HHS R01 HL117491NHLBI NIH HHS R01 HL129778NHLBI NIH HHS R01 HL147527
6 · The paper itself

Abstract

objectiveApo (apolipoprotein) CIII mediates the metabolism of triglyceride (TG)-rich lipoproteins. High levels of plasma apoCIII are positively correlated with the plasma TG levels and increase the cardiovascular risk. However, whether apoCIII is directly involved in the development of atherosclerosis has not been fully elucidated. Approach and Results: To examine the possible roles of apoCIII in lipoprotein metabolism and atherosclerosis, we generated apoCIII KO (knockout) rabbits using ZFN (zinc finger nuclease) technique. On a normal standard diet, apoCIII KO rabbits exhibited significantly lower plasma levels of TG than those of WT (wild type) rabbits while total cholesterol and HDL (high-density lipoprotein) cholesterol levels were unchanged. Analysis of lipoproteins isolated by sequential ultracentrifugation revealed that reduced plasma TG levels in KO rabbits were accompanied by prominent reduction of VLDLs (very-low-density lipoproteins) and IDLs (intermediate-density lipoproteins). In addition, KO rabbits showed faster TG clearance rate after intravenous fat load than WT rabbits. On a cholesterol-rich diet, KO rabbits exhibited constantly and significantly lower levels of plasma total cholesterol and TG than WT rabbits, which was caused by a remarkable reduction of β-VLDLs-the major atherogenic lipoproteins. β-VLDLs of KO rabbits showed higher uptake by cultured hepatocytes and were cleared faster from the circulation than β-VLDLs isolated from WT rabbits. Both aortic and coronary atherosclerosis was significantly reduced in KO rabbits compared with WT rabbits.

conclusionsThese results indicate that apoCIII deficiency facilitates TG-rich lipoprotein catabolism, and therapeutic inhibition of apoCIII expression may become a novel means not only for the treatment of hyperlipidemia but also for atherosclerosis.

Indexed as

AnimalsAnimals, Genetically ModifiedAortic DiseasesApolipoprotein C-IIIAtherosclerosisBiomarkersCholesterol, HDLCholesterol, VLDLCoronary Artery DiseaseDisease Models, AnimalFemaleHepatocytesHep G2 CellsHumansLipoproteins, IDLLiverApolipoprotein C-IIIBiomarkersCholesterol, HDLCholesterol, VLDLLipoproteins, IDLTriglyceridesaortaapolipoprotein CIIIatherosclerosishyperlipidemiaslipoproteins

Identifiers

PMID32757647
PMCPMC7484272
OpenAlexW3047483359

What OpenQuestion holds

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LicenceTDM
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 OpenQuestion graph.