Evidence map›Paper›PMID 33021977›Full record

ArticlePLoS neglected tropical diseases2020

Genome-scale metabolic models highlight stage-specific differences in essential metabolic pathways in Trypanosoma cruzi.

Isabel S Shiratsubaki, Xin Fang, Rodolpho O O Souza, Bernhard O Palsson, Ariel M Silber, Jair L Siqueira-Neto

Open access · goldAbstract read
In one paragraph

Article in PLoS neglected tropical diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.7field-weighted citation impact, top 32% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Article
  2. Glycosomal Phosphoenolpyruvate Carboxykinase CRISPR/Cas9-Deletion and Its Role in Trypanosoma cruzi Metacyclogenesis and Infectivity in Mammalian Host.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. Article
  4. Article
  5. Genome-scale knockout simulation and clustering analysis of drug-resistant breast cancer cells reveal drug sensitization targets.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  6. Review
  7. Review
  8. Article
  9. Virulence · 2022
    Article
  10. Metabolic Alteration ofPathogens (Basel, Switzerland) · 2022
    Article
  11. Review
  12. 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

6 authors at 3 institutions in 3 countries.

Isabel S ShiratsubakiSkaggs School of Pharmacy and Pharmaceutical Sciences, UC San Diego, La Jolla, California, United States of America.
Xin FangDepartment of Bioengineering, UC San Diego, La Jolla, California, United States of America.
Rodolpho O O SouzaLaboratory of Biochemistry of Tryps - LaBTryps, Department of Parasitology, Institute of Biomedical Science, University of São Paulo, São Paulo, São Paulo, Brazil.ORCID 0000-0003-1215-8553
Bernhard O PalssonDepartment of Bioengineering, UC San Diego, La Jolla, California, United States of America.ORCID 0000-0003-2357-6785
Ariel M SilberLaboratory of Biochemistry of Tryps - LaBTryps, Department of Parasitology, Institute of Biomedical Science, University of São Paulo, São Paulo, São Paulo, Brazil.ORCID 0000-0003-4528-4732
Jair L Siqueira-NetoSkaggs School of Pharmacy and Pharmaceutical Sciences, UC San Diego, La Jolla, California, United States of America.ORCID 0000-0001-9574-8174
University of California San Diego · USUniversidade de São Paulo · BRNovo Nordisk Foundation · DK

Funding

Medical Research Council MR/P027989/1
6 · The paper itself

Abstract

Chagas disease is a neglected tropical disease and a leading cause of heart failure in Latin America caused by a protozoan called Trypanosoma cruzi. This parasite presents a complex multi-stage life cycle. Anti-Chagas drugs currently available are limited to benznidazole and nifurtimox, both with severe side effects. Thus, there is a need for alternative and more efficient drugs. Genome-scale metabolic models (GEMs) can accurately predict metabolic capabilities and aid in drug discovery in metabolic genes. This work developed an extended GEM, hereafter referred to as iIS312, of the published and validated T. cruzi core metabolism model. From iIS312, we then built three stage-specific models through transcriptomics data integration, and showed that epimastigotes present the most active metabolism among the stages (see S1-S4 GEMs). Stage-specific models predicted significant metabolic differences among stages, including variations in flux distribution in core metabolism. Moreover, the gene essentiality predictions suggest potential drug targets, among which some have been previously proven lethal, including glutamate dehydrogenase, glucokinase and hexokinase. To validate the models, we measured the activity of enzymes in the core metabolism of the parasite at different stages, and showed the results were consistent with model predictions. Our results represent a potential step forward towards the improvement of Chagas disease treatment. To our knowledge, these stage-specific models are the first GEMs built for the stages Amastigote and Trypomastigote. This work is also the first to present an in silico GEM comparison among different stages in the T. cruzi life cycle.

Indexed as

Drug DiscoveryLife Cycle StagesMetabolic Networks and PathwaysProteomicsProtozoan ProteinsTrypanocidal AgentsTrypanosoma cruziProtozoan ProteinsTrypanocidal Agents

Identifiers

PMID33021977
PMCPMC7567352
OpenAlexW3092203874

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.