Evidence map›Paper›PMID 28468832›Full record

ReviewPhysiological reviews2017

LITTLE FISH, BIG DATA: ZEBRAFISH AS A MODEL FOR CARDIOVASCULAR AND METABOLIC DISEASE.

Philipp Gut, Sven Reischauer, Didier Y R Stainier, Rima Arnaout

Abstract readReview
In one paragraph

Review in Physiological reviews, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 163 papers.

0numbers the graph read from it
0cells of the map it votes in
163citing papers in PubMed
–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

163 citing papers in PubMed.

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103 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

4 authors.

Philipp GutNestlé Institute of Health Sciences, EPFL Innovation Park, Lausanne, Switzerland; Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany; and Cardiovascular Research Institute and Division of Cardiology, Department of Medicine, University of California San Francisco, San Francisco, California.
Sven ReischauerNestlé Institute of Health Sciences, EPFL Innovation Park, Lausanne, Switzerland; Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany; and Cardiovascular Research Institute and Division of Cardiology, Department of Medicine, University of California San Francisco, San Francisco, California.
Didier Y R StainierNestlé Institute of Health Sciences, EPFL Innovation Park, Lausanne, Switzerland; Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany; and Cardiovascular Research Institute and Division of Cardiology, Department of Medicine, University of California San Francisco, San Francisco, California.
Rima ArnaoutNestlé Institute of Health Sciences, EPFL Innovation Park, Lausanne, Switzerland; Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany; and Cardiovascular Research Institute and Division of Cardiology, Department of Medicine, University of California San Francisco, San Francisco, California.

Funding

Genetics and Structure of Trabecular Myocardium in Development and DiseaseK08HL125945 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ARNAOUT, RIMA · 2015 to 2019
$863k
NHLBI NIH HHS K08 HL125945
6 · The paper itself

Abstract

The burden of cardiovascular and metabolic diseases worldwide is staggering. The emergence of systems approaches in biology promises new therapies, faster and cheaper diagnostics, and personalized medicine. However, a profound understanding of pathogenic mechanisms at the cellular and molecular levels remains a fundamental requirement for discovery and therapeutics. Animal models of human disease are cornerstones of drug discovery as they allow identification of novel pharmacological targets by linking gene function with pathogenesis. The zebrafish model has been used for decades to study development and pathophysiology. More than ever, the specific strengths of the zebrafish model make it a prime partner in an age of discovery transformed by big-data approaches to genomics and disease. Zebrafish share a largely conserved physiology and anatomy with mammals. They allow a wide range of genetic manipulations, including the latest genome engineering approaches. They can be bred and studied with remarkable speed, enabling a range of large-scale phenotypic screens. Finally, zebrafish demonstrate an impressive regenerative capacity scientists hope to unlock in humans. Here, we provide a comprehensive guide on applications of zebrafish to investigate cardiovascular and metabolic diseases. We delineate advantages and limitations of zebrafish models of human disease and summarize their most significant contributions to understanding disease progression to date.

Indexed as

AnimalsAnimals, Genetically ModifiedCardiovascular AgentsCardiovascular DiseasesDisease Models, AnimalDrug DiscoveryGenetic Predisposition to DiseaseHumansMetabolic DiseasesPhenotypeSpecies SpecificityZebrafishCardiovascular Agents

Identifiers

PMID28468832
PMCPMC5817164

What OpenQuestion holds

Textmetadata
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.