Evidence map›Paper›PMID 28598490›Full record

ArticleMolecular medicine (Cambridge, Mass.)2017

Development of a zebrafish sepsis model for high-throughput drug discovery.

Anju Mary Philip, Youdong Wang, Antonio Mauro, Suzan El-Rass, John C Marshall, Warren L Lee, Arthur S Slutsky, Claudia C dosSantos, Xiao-Yan Wen

Open access · goldAbstract read
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

35 citing papers in PubMed, 59 citations in OpenAlex.

  1. Article
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  3. A teleost-specific oxygen-immunity axis where FIH activates NF-κB via competitive IκBα binding.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Spatially structured inflammatory response in the presence of a uniform stimulus.Proceedings of the National Academy of Sciences of the United States of America · 2026
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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

9 authors at 1 institution in 1 country.

Anju Mary PhilipZebrafish Centre for Advanced Drug Discovery, St. Michael's Hospital, 209 Victoria St, Toronto, Ontario, Canada M5B 1T8.
Youdong WangZebrafish Centre for Advanced Drug Discovery, St. Michael's Hospital, 209 Victoria St, Toronto, Ontario, Canada M5B 1T8.
Antonio MauroZebrafish Centre for Advanced Drug Discovery, St. Michael's Hospital, 209 Victoria St, Toronto, Ontario, Canada M5B 1T8.
Suzan El-RassZebrafish Centre for Advanced Drug Discovery, St. Michael's Hospital, 209 Victoria St, Toronto, Ontario, Canada M5B 1T8.
John C MarshallZebrafish Centre for Advanced Drug Discovery, St. Michael's Hospital, 209 Victoria St, Toronto, Ontario, Canada M5B 1T8.
Warren L LeeZebrafish Centre for Advanced Drug Discovery, St. Michael's Hospital, 209 Victoria St, Toronto, Ontario, Canada M5B 1T8.
Arthur S SlutskyZebrafish Centre for Advanced Drug Discovery, St. Michael's Hospital, 209 Victoria St, Toronto, Ontario, Canada M5B 1T8.
Claudia C dosSantosZebrafish Centre for Advanced Drug Discovery, St. Michael's Hospital, 209 Victoria St, Toronto, Ontario, Canada M5B 1T8.
Xiao-Yan WenZebrafish Centre for Advanced Drug Discovery, St. Michael's Hospital, 209 Victoria St, Toronto, Ontario, Canada M5B 1T8.
St. Michael's Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Sepsis is a leading cause of death worldwide. Current treatment modalities remain largely supportive. Intervention strategies focused on inhibiting specific mediators of the inflammatory host response have been largely unsuccessful, a consequence of an inadequate understanding of the complexity and heterogeneity of the innate immune response. Moreover, the conventional drug development pipeline is time consuming and expensive and the low success rates associated with cell-based screens underline the need for whole organism screening strategies, especially for complex pathological processes. Here, we established an LPS-induced zebrafish endotoxemia model, which exhibits the major hallmarks of human sepsis including, edema and tissue/organ damage, increased vascular permeability and vascular leakage accompanied by an altered expression of cellular junction proteins, increased cytokine expression, immune cell activation and ROS production, reduced circulation and increased platelet aggregation. We tested the suitability of the model for phenotype-based drug screening using three primary readouts: mortality, vascular leakage, and ROS production. Preliminary screening identified fasudil, a drug known to protect against vascular leakage in murine models, as a lead hit thereby validating the utility of our model for sepsis drug screens. This zebrafish sepsis model has the potential to rapidly analyze sepsis associated pathologies and cellular processes in the whole organism, as well as to screen and validate large numbers of compounds that can modify sepsis pathology in

Indexed as

Disease Models, AnimalDrug DiscoveryHigh-Throughput Screening AssaysLipopolysaccharidesSepsisZebrafishAnimalsCytokinesEmbryo, NonmammalianMacrophagesNeutrophilsPhenotypeReactive Oxygen SpeciesCytokinesLipopolysaccharidesReactive Oxygen Speciesendothelial dysfunctionendotoxinlipopolysaccharidesepsisvascular leakagezebrafish

Identifiers

PMID28598490
PMCPMC5522968
OpenAlexW2738924000

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.