Evidence map›Paper›PMID 25582694›Full record

ArticleThe American journal of tropical medicine and hygiene2015

AKT network of genes and impaired myocardial contractility during murine acute Chagasic myocarditis.

Andrés F Henao-Martínez, Anne Hermetet Agler, Alan M Watson, Corinne Hennessy, Elizabeth Davidson, Kim Demos-Davies, Timothy A McKinsey, Michael Wilson, David A Schwartz, Ivana V Yang

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of tropical medicine and hygiene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

4 citing papers in PubMed, 6 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

10 authors at 2 institutions in 1 country.

Andrés F Henao-MartínezDivision of Infectious Diseases and Departments of Medicine and Immunology, University of Colorado, Denver, Colorado; Department of Epidemiology, Colorado School of Public Health, Denver, Colorado; Department of Pathology, Denver Health, Denver, Colorado andres.henaomartinez@ucdenver.edu.
Anne Hermetet AglerDivision of Infectious Diseases and Departments of Medicine and Immunology, University of Colorado, Denver, Colorado; Department of Epidemiology, Colorado School of Public Health, Denver, Colorado; Department of Pathology, Denver Health, Denver, Colorado.
Alan M WatsonDivision of Infectious Diseases and Departments of Medicine and Immunology, University of Colorado, Denver, Colorado; Department of Epidemiology, Colorado School of Public Health, Denver, Colorado; Department of Pathology, Denver Health, Denver, Colorado.
Corinne HennessyDivision of Infectious Diseases and Departments of Medicine and Immunology, University of Colorado, Denver, Colorado; Department of Epidemiology, Colorado School of Public Health, Denver, Colorado; Department of Pathology, Denver Health, Denver, Colorado.
Elizabeth DavidsonDivision of Infectious Diseases and Departments of Medicine and Immunology, University of Colorado, Denver, Colorado; Department of Epidemiology, Colorado School of Public Health, Denver, Colorado; Department of Pathology, Denver Health, Denver, Colorado.
Kim Demos-DaviesDivision of Infectious Diseases and Departments of Medicine and Immunology, University of Colorado, Denver, Colorado; Department of Epidemiology, Colorado School of Public Health, Denver, Colorado; Department of Pathology, Denver Health, Denver, Colorado.
Timothy A McKinseyDivision of Infectious Diseases and Departments of Medicine and Immunology, University of Colorado, Denver, Colorado; Department of Epidemiology, Colorado School of Public Health, Denver, Colorado; Department of Pathology, Denver Health, Denver, Colorado.
Michael WilsonDivision of Infectious Diseases and Departments of Medicine and Immunology, University of Colorado, Denver, Colorado; Department of Epidemiology, Colorado School of Public Health, Denver, Colorado; Department of Pathology, Denver Health, Denver, Colorado.
David A SchwartzDivision of Infectious Diseases and Departments of Medicine and Immunology, University of Colorado, Denver, Colorado; Department of Epidemiology, Colorado School of Public Health, Denver, Colorado; Department of Pathology, Denver Health, Denver, Colorado.
Ivana V YangDivision of Infectious Diseases and Departments of Medicine and Immunology, University of Colorado, Denver, Colorado; Department of Epidemiology, Colorado School of Public Health, Denver, Colorado; Department of Pathology, Denver Health, Denver, Colorado.
Colorado Department of Public Health and Environment · USUniversity of Colorado Health · US

Funding

Colorado Clinical and Translational Sciences InstituteUL1TR001082 · NCATS · UNIVERSITY OF COLORADO DENVER · PI SOKOL, RONALD J. · 2013 to 2017
$48.0M
Regulation of Cardiac Signaling by Class I Histone DeacetylasesR01HL116848 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI MCKINSEY, TIMOTHY · 2013 to 2021
$3.1M
NCATS NIH HHS UL1 TR001082NHLBI NIH HHS R01 HL116848
6 · The paper itself

Abstract

Chagasic disease is associated with high morbidity in Latin America. Acute Chagasic myocarditis is consistently found in acute infections, but little is known about its contribution to chronic cardiomyopathy. The aim of the study was to phenotypically characterize two strains of mice with differential Chagas infection susceptibility and correlate strain myocarditis phenotypes with heart tissue gene expression. C57BL/6J and Balb/c mice were injected intraperitoneally with 0 or 150-200 tissue-derived trypomastigotes (Tulahuen strain). Echocardiograms, brain natriuretic peptide, and troponin were measured. Heart tissue was harvested for histopathological analysis and gene expression profiling on microarrays. Genes differently expressed between infected Balb/c and C57BL/6J mice were identified. Echocardiograms showed differences in Balb/c versus C57BL/6J infected mice in heart rate (413 versus 476 beats per minute; P = 0.0001), stroke volume (31.9 ± 9.3 versus 39.2 ± 5.5 μL; P = 0.03), and cardiac output (13.1 ± 3.5 versus 18.7 ± 3.2 μL/min; P = 0.002). Gene expression at 4 weeks analysis showed 32 statistically significant (q value < 0.05) differentially expressed genes between infected Balb/c and C57BL/6J mice that were enriched for genes related to the protein kinase B (AKT) pathway. These specific phenotypic features of cardiac response during acute Chagasic myocarditis may, in part, be related to host AKT network regulation.

Indexed as

AnimalsChagas CardiomyopathyGene Expression RegulationMiceMice, Inbred BALB CMice, Inbred C57BLMyocardial ContractionProto-Oncogene Proteins c-aktTrypanosoma cruziProto-Oncogene Proteins c-akt

Identifiers

PMID25582694
PMCPMC4350542
OpenAlexW2101116613

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.