Evidence map›Paper›PMID 28322302›Full record

ArticleScientific reports2017

Mechanistic Insights into the Anti-angiogenic Activity of Trypanosoma cruzi Protein 21 and its Potential Impact on the Onset of Chagasic Cardiomyopathy.

Samuel Cota Teixeira, Daiana Silva Lopes, Sarah Natalie Cirilo Gimenes, Thaise Lara Teixeira, Marcelo Santos da Silva, Rebecca Tavares E Silva Brígido, Felipe Andrés Cordero da Luz, Aline Alves da Silva, Makswell Almeida Silva, Pilar Veras Florentino and 7 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

14 citing papers in PubMed, 40 citations in OpenAlex.

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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

17 authors at 3 institutions in 1 country.

Samuel Cota TeixeiraLaboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, MG, Brasil.
Daiana Silva LopesLaboratório de Bioquímica e Toxinas Animais, Instituto de Genética e Bioquímica, Universidade Federal de Uberlândia, MG, Brasil.
Sarah Natalie Cirilo GimenesLaboratório de Bioquímica e Toxinas Animais, Instituto de Genética e Bioquímica, Universidade Federal de Uberlândia, MG, Brasil.
Thaise Lara TeixeiraLaboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, MG, Brasil.
Marcelo Santos da SilvaCenter of Toxins, Immune Response and Cell Signaling (CeTICS), Instituto Butantan, São Paulo, São Paulo, Brasil.
Rebecca Tavares E Silva BrígidoLaboratório de Patologia Molecular e Biotecnologia do Centro de Referência Nacional em Dermatologia Sanitária/Hanseníase, Faculdade de Medicina, Universidade Federal de Uberlândia, MG, Brasil.
Felipe Andrés Cordero da LuzLaboratório de Osteoimunologia e Imunologia dos Tumores, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, MG, Brasil.
Aline Alves da SilvaLaboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, MG, Brasil.
Makswell Almeida SilvaLaboratório de Bioquímica e Toxinas Animais, Instituto de Genética e Bioquímica, Universidade Federal de Uberlândia, MG, Brasil.
Pilar Veras FlorentinoDepartamento de Microbiologia Imunologia e Parasitologia, Escola Paulista de Medicina, Universidade Federal de São Paulo, SP, Brasil.
Paula Cristina Brígido TavaresLaboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, MG, Brasil.
Marlus Alves Dos SantosLaboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, MG, Brasil.
Veridiana de Melo Rodrigues ÁvilaLaboratório de Bioquímica e Toxinas Animais, Instituto de Genética e Bioquímica, Universidade Federal de Uberlândia, MG, Brasil.
Marcelo José Barbosa SilvaLaboratório de Osteoimunologia e Imunologia dos Tumores, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, MG, Brasil.
Maria Carolina EliasCenter of Toxins, Immune Response and Cell Signaling (CeTICS), Instituto Butantan, São Paulo, São Paulo, Brasil.
Renato Arruda MortaraDepartamento de Microbiologia Imunologia e Parasitologia, Escola Paulista de Medicina, Universidade Federal de São Paulo, SP, Brasil.
Claudio Vieira da SilvaLaboratório de Tripanosomatídeos, Departamento de Imunologia, Instituto de Ciências Biomédicas, Universidade Federal de Uberlândia, MG, Brasil.
Universidade Federal de Uberlândia · BRInstituto Butantan · BRUniversidade Federal de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic chagasic cardiomyopathy (CCC) is arguably the most important form of the Chagas Disease, caused by the intracellular protozoan Trypanosoma cruzi; it is estimated that 10-30% of chronic patients develop this clinical manifestation. The most common and severe form of CCC can be related to ventricular abnormalities, such as heart failure, arrhythmias, heart blocks, thromboembolic events and sudden death. Therefore, in this study, we proposed to evaluate the anti-angiogenic activity of a recombinant protein from T. cruzi named P21 (rP21) and the potential impact of the native protein on CCC. Our data suggest that the anti-angiogenic activity of rP21 depends on the protein's direct interaction with the CXCR4 receptor. This capacity is likely related to the modulation of the expression of actin and angiogenesis-associated genes. Thus, our results indicate that T. cruzi P21 is an attractive target for the development of innovative therapeutic agents against CCC.

Indexed as

ActinsAngiogenesis InhibitorsAnimalsCell LineCell ProliferationChagas DiseaseCytoskeletonEndothelial CellsExtracellular MatrixGene Expression RegulationHumansMiceModels, BiologicalNeovascularization, PathologicProtein MultimerizationProtozoan ProteinsActinsAngiogenesis InhibitorsCXCR4 protein, humanProtozoan ProteinsReceptors, CXCR4Recombinant Proteins

Identifiers

PMID28322302
PMCPMC5359584
OpenAlexW2601706075

What OpenQuestion holds

Textmetadata
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.