Evidence map›Paper›PMID 25210230›Full record

ReviewMediators of inflammation2014

Chagas disease cardiomyopathy: immunopathology and genetics.

Edecio Cunha-Neto, Christophe Chevillard

Open access · goldAbstract readReview
In one paragraph

Review in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
122citing papers in PubMed, 7 pooled it
11.8field-weighted citation impact, top 1% 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

122 citing papers in PubMed, 7 syntheses or guidelines pooled it, 211 citations in OpenAlex.

  1. Guideline
  2. Galectin-3 and fibrosis intensity in Chronic Chagas Cardiomyopathy: a systematic review.Revista do Instituto de Medicina Tropical de Sao Paulo · 2022
    Pooled it
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  6. Pharmacological interventions for treating heart failure in patients with Chagas cardiomyopathy.The Cochrane database of systematic reviews · 2016 · on this map
    Pooled it
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  8. Trial
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  13. Review
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62 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

2 authors at 2 institutions in 2 countries.

Edecio Cunha-NetoHeart Institute (InCor), University of São Paulo School of Medicine, Avenida Dr. Enéas de Carvalho Aguiar, 44 Bloco 2 9° Andar, 05406-000 São Paulo, SP, Brazil ; Institute for Investigation in Immunology (iii), INCT, São Paulo, SP, Brazil ; Division of Clinical Immunology and Allergy, University of São Paulo School of Medicine, 05406-000 São Paulo, SP, Brazil.ORCID 0000-0002-3699-3345
Christophe ChevillardAix-Marseille Université, INSERM, GIMP UMR_S906, 13385 Marseille, France.
Inserm · FRUniversidade de São Paulo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chagas disease, caused by the protozoan Trypanosoma cruzi, is endemic in Latin America and affects ca. 10 million people worldwide. About 30% of Chagas disease patients develop chronic Chagas disease cardiomyopathy (CCC), a particularly lethal inflammatory cardiomyopathy that occurs decades after the initial infection, while most patients remain asymptomatic. Mortality rate is higher than that of noninflammatory cardiomyopathy. CCC heart lesions present a Th1 T-cell-rich myocarditis, with cardiomyocyte hypertrophy and prominent fibrosis. Data suggest that the myocarditis plays a major pathogenetic role in disease progression. Major unmet goals include the thorough understanding of disease pathogenesis and therapeutic targets and identification of prognostic genetic factors. Chagas disease thus remains a neglected disease, with no vaccines or antiparasitic drugs proven efficient in chronically infected adults, when most patients are diagnosed. Both familial aggregation of CCC cases and the fact that only 30% of infected patients develop CCC suggest there might be a genetic component to disease susceptibility. Moreover, previous case-control studies have identified some genes associated to human susceptibility to CCC. In this paper, we will review the immunopathogenesis and genetics of Chagas disease, highlighting studies that shed light on the differential progression of Chagas disease patients to CCC.

Indexed as

AnimalsChagas CardiomyopathyHumans

Identifiers

PMID25210230
PMCPMC4152981
OpenAlexW2030405016

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.