Evidence map›Paper›PMID 26914991›Full record

ReviewCell biochemistry and function2016

Large animal models of cardiovascular disease.

H G Tsang, N A Rashdan, C B A Whitelaw, B M Corcoran, K M Summers, V E MacRae

Abstract readReview
In one paragraph

Review in Cell biochemistry and function, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
82citing papers in PubMed, 4 pooled it
–field-weighted citation impact
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

82 citing papers in PubMed, 4 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Preclinical Large AnimalCurrent cardiology reviews · 2023
    Pooled it
  4. Coenzyme QFrontiers in cardiovascular medicine · 2022
    Pooled it
  5. Review
  6. A Novel Minimally Invasive Porcine Model of Functional Tricuspid Regurgitation.Journal of cardiovascular development and disease · 2026
    Article
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22 more citing papers are in PubMed but not listed here.

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

6 authors.

H G TsangThe Roslin Institute, Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Midlothian, SCT, UK.
N A RashdanThe Roslin Institute, Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Midlothian, SCT, UK.
C B A WhitelawThe Roslin Institute, Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Midlothian, SCT, UK.
B M CorcoranRoyal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Midlothian, SCT, UK.
K M SummersThe Roslin Institute, Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Midlothian, SCT, UK.
V E MacRaeThe Roslin Institute, Royal (Dick) School of Veterinary Studies, The University of Edinburgh, Easter Bush, Midlothian, SCT, UK.

Funding

Biotechnology and Biological Sciences Research Council BB/F023928/1Biotechnology and Biological Sciences Research Council BB/J004316/1Biotechnology and Biological Sciences Research Council BB/J01446X/1Biotechnology and Biological Sciences Research Council BBS/E/D/20211553Biotechnology and Biological Sciences Research Council BBS/E/R/00001608
6 · The paper itself

Abstract

The human cardiovascular system is a complex arrangement of specialized structures with distinct functions. The molecular landscape, including the genome, transcriptome and proteome, is pivotal to the biological complexity of both normal and abnormal mammalian processes. Despite our advancing knowledge and understanding of cardiovascular disease (CVD) through the principal use of rodent models, this continues to be an increasing issue in today's world. For instance, as the ageing population increases, so does the incidence of heart valve dysfunction. This may be because of changes in molecular composition and structure of the extracellular matrix, or from the pathological process of vascular calcification in which bone-formation related factors cause ectopic mineralization. However, significant differences between mice and men exist in terms of cardiovascular anatomy, physiology and pathology. In contrast, large animal models can show considerably greater similarity to humans. Furthermore, precise and efficient genome editing techniques enable the generation of tailored models for translational research. These novel systems provide a huge potential for large animal models to investigate the regulatory factors and molecular pathways that contribute to CVD in vivo. In turn, this will help bridge the gap between basic science and clinical applications by facilitating the refinement of therapies for cardiovascular disease.

Indexed as

Cardiovascular DiseasesDisease Models, AnimalAnimalsHumansaortic stenosiscalcific aortic valve diseasecardiovascular diseasegenetic engineeringlarge animal modelsMarfan syndromevascular calcification

Identifiers

PMID26914991
PMCPMC4834612

What OpenQuestion holds

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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.