Evidence map›Paper›PMID 26044956›Full record

ArticleDisease models & mechanisms2015

Apoc2 loss-of-function zebrafish mutant as a genetic model of hyperlipidemia.

Chao Liu, Keith P Gates, Longhou Fang, Marcelo J Amar, Dina A Schneider, Honglian Geng, Wei Huang, Jungsu Kim, Jennifer Pattison, Jian Zhang and 4 more

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

Article in Disease models & mechanisms, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

47 citing papers in PubMed, 69 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Zebrafish ApoB-Containing Lipoprotein Metabolism: A Closer Look.Arteriosclerosis, thrombosis, and vascular biology · 2024
    Review
  8. Article
  9. Pancreatitis as a Main Consequence ofInternational journal of genomics · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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

14 authors at 5 institutions in 2 countries.

Chao LiuDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
Keith P GatesSanford Children's Health Research Center, Programs in Genetic Disease and Development and Aging, and Stem Cell and Regenerative Biology, Sanford-Burnham Medical Research Institute, La Jolla, CA, USA.
Longhou FangDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
Marcelo J AmarLipoprotein Metabolism Section, Cardiopulmonary Branch, NHLBI, NIH, Bethesda, MD, USA.
Dina A SchneiderDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
Honglian GengDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
Wei HuangDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
Jungsu KimDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
Jennifer PattisonDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
Jian ZhangState Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China.
Joseph L WitztumDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
Alan T RemaleyLipoprotein Metabolism Section, Cardiopulmonary Branch, NHLBI, NIH, Bethesda, MD, USA.
P Duc DongSanford Children's Health Research Center, Programs in Genetic Disease and Development and Aging, and Stem Cell and Regenerative Biology, Sanford-Burnham Medical Research Institute, La Jolla, CA, USA.
Yury I MillerDivision of Endocrinology and Metabolism, Department of Medicine, University of California, San Diego, La Jolla, CA, USA yumiller@ucsd.edu.
University of California, San Diego · USSanford Burnham Prebys Medical Discovery Institute · USChinese Academy of Sciences · CNNational Heart Lung and Blood Institute · USNational Institutes of Health · US

Funding

ROLE OF LIPOXYGENASES IN ATHEROGENESIS IN DIABETES MELLITUSP01HL055798 · NHLBI · UNIVERSITY OF VIRGINIA CHARLOTTESVILLE · PI MCNAMARA, COLEEN A · 1995 to 2016
$28.4M
Transcriptional GenomicsP01HL088093 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI WITZTUM, JOSEPH L. · 2008 to 2018
$26.4M
Unlocking Regenerative Potential through in Vivo Genetic ReprogrammingDP2DK098092 · NIDDK · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI DONG, P. DUC SI · 2012 to 2012
$2.9M
Zebrafish models of vascular inflammation and atherosclerosisR01HL093767 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MILLER, YURY · 2009 to 2014
$2.5M
NHLBI NIH HHS HL055798NHLBI NIH HHS HL088093NHLBI NIH HHS HL093767NHLBI NIH HHS P01 HL055798NHLBI NIH HHS P01 HL088093NHLBI NIH HHS R01 HL093767NIDDK NIH HHS DP2 DK098092NINDS NIH HHS P30NS0471010
6 · The paper itself

Abstract

Apolipoprotein C-II (APOC2) is an obligatory activator of lipoprotein lipase. Human patients with APOC2 deficiency display severe hypertriglyceridemia while consuming a normal diet, often manifesting xanthomas, lipemia retinalis and pancreatitis. Hypertriglyceridemia is also an important risk factor for development of cardiovascular disease. Animal models to study hypertriglyceridemia are limited, with no Apoc2-knockout mouse reported. To develop a genetic model of hypertriglyceridemia, we generated an apoc2 mutant zebrafish characterized by the loss of Apoc2 function. apoc2 mutants show decreased plasma lipase activity and display chylomicronemia and severe hypertriglyceridemia, which closely resemble the phenotype observed in human patients with APOC2 deficiency. The hypertriglyceridemia in apoc2 mutants is rescued by injection of plasma from wild-type zebrafish or by injection of a human APOC2 mimetic peptide. Consistent with a previous report of a transient apoc2 knockdown, apoc2 mutant larvae have a minor delay in yolk consumption and angiogenesis. Furthermore, apoc2 mutants fed a normal diet accumulate lipid and lipid-laden macrophages in the vasculature, which resemble early events in the development of human atherosclerotic lesions. In addition, apoc2 mutant embryos show ectopic overgrowth of pancreas. Taken together, our data suggest that the apoc2 mutant zebrafish is a robust and versatile animal model to study hypertriglyceridemia and the mechanisms involved in the pathogenesis of associated human diseases.

Indexed as

Models, GeneticAgingAmino Acid SequenceAnimalsApolipoprotein C-IIBase SequenceBlood VesselsDietDisease Models, AnimalEndonucleasesHumansHyperlipidemiasInjectionsLarvaLipoproteinsMolecular Sequence DataApoc2 protein, zebrafishApolipoprotein C-IIEndonucleasesLipoproteinsPeptidesTrans-ActivatorsTriglyceridesZebrafish ProteinsAPOC2Apolipoprotein C-IIHyperlipidemiaLipoprotein lipaseZebrafish

Identifiers

PMID26044956
PMCPMC4527288
OpenAlexW2119368892

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.