Evidence map›Paper›PMID 31779098›Full record

ArticleInternational journal of molecular sciences2019

Heterozygous Ldlr-Deficient Hamster as a Model to Evaluate the Efficacy of PCSK9 Antibody in Hyperlipidemia and Atherosclerosis.

Yue Wu, Ming-Jiang Xu, Zhiyou Cao, Chun Yang, Jinjie Wang, Bijue Wang, Jian Liu, Yuhui Wang, Xunde Xian, Fang Zhang and 2 more

Open access · goldFull text readComparative Study
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 10% 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

9 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Rodent Models for Atherosclerosis.International journal of molecular sciences · 2025
    Review
  4. Article
  5. Review
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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

12 authors at 1 institution in 1 country.

Yue WuNovo Nordisk Research Centre China, Novo Nordisk A/S, Beijing 102206, China.
Ming-Jiang XuNovo Nordisk Research Centre China, Novo Nordisk A/S, Beijing 102206, China.
Zhiyou CaoNovo Nordisk Research Centre China, Novo Nordisk A/S, Beijing 102206, China.
Chun YangInstitute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University, Beijing 100191, China.
Jinjie WangInstitute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University, Beijing 100191, China.
Bijue WangNovo Nordisk Research Centre China, Novo Nordisk A/S, Beijing 102206, China.
Jian LiuNovo Nordisk Research Centre China, Novo Nordisk A/S, Beijing 102206, China.
Yuhui WangInstitute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University, Beijing 100191, China.
Xunde XianInstitute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University, Beijing 100191, China.ORCID 0000-0003-3059-1254
Fang ZhangNovo Nordisk Research Centre China, Novo Nordisk A/S, Beijing 102206, China.
George LiuInstitute of Cardiovascular Sciences, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Peking University, Beijing 100191, China.
Xiaoli ChenNovo Nordisk Research Centre China, Novo Nordisk A/S, Beijing 102206, China.
Peking University · CN

Funding

National Key Research and Development Program of China 2016YFE0126000National Science Foundation of China 31520103909; 81270367; 81570787; 81770449
6 · The paper itself

Abstract

Proprotein convertase subtilisin/kexin type 9 (PCSK9) plays a key role in cholesterol homeostasis and atherogenesis. However, there are only limited rodent models, with a functional low-density lipoprotein receptor (LDLR) pathway and cholesteryl ester transfer protein (CETP) to evaluate the drug candidates targeting the PCSK9/LDLR pathway, that are translatable to humans. Here, by using our recently generated LDLR heterozygote (

Indexed as

AnimalsAntibodies, Monoclonal, HumanizedAtherosclerosisCholesterol, LDLCricetinaeDiet, High-FatDisease Models, AnimalEzetimibeHeterozygoteHumansHyperlipidemiasMalePCSK9 InhibitorsReceptors, LDLTreatment OutcomeTriglyceridesAntibodies, Monoclonal, HumanizedCholesterol, LDLevolocumabEzetimibePCSK9 InhibitorsReceptors, LDLTriglyceridesanimal modelatherosclerosisdyslipidemialow-density lipoproteinlow-density lipoprotein receptorproprotein convertase subtilisin/kexin type 9

Identifiers

PMID31779098
PMCPMC6929182
OpenAlexW2989618240

What OpenQuestion holds

Textfull text, public
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.