ReviewMediators of inflammation2014
Chagas disease: still many unsolved issues.
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 21 papers.
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.
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.
Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- Therapeutical Potential and Immunomodulatory Profile ofACS infectious diseases · 2025Article
- Nasal vaccination againstFrontiers in immunology · 2025Article
- Intranasal Trans-Sialidase Vaccine Mitigates Acute and Chronic Pathology in a Preclinical Oral Chagas Disease Model.Vaccines · 2024Article
- Antimicrobial activity of NK cells to Trypanosoma cruzi infected human primary Keratinocytes.PLoS neglected tropical diseases · 2024Article
- Localized cardiac small molecule trajectories and persistent chemical sequelae in experimental Chagas disease.Nature communications · 2023Article
- Vaccine-linked chemotherapy improves cardiac structure and function in a mouse model of chronic Chagas disease.Frontiers in cellular and infection microbiology · 2023Article
- Immunomodulatory proteins from hookworms reduce cardiac inflammation and modulate regulatory responses in a mouse model of chronicFrontiers in parasitology · 2023Article
- In Chagas disease, transforming growth factor beta neutralization reducesFrontiers in cellular and infection microbiology · 2022Article
- Absence of Bim sensitizes mice to experimental Trypanosoma cruzi infection.Cell death & disease · 2021Article
- A Trypsin Inhibitor fromAntibiotics (Basel, Switzerland) · 2020Article
- Pathology and Pathogenesis of Chagas Heart Disease.Annual review of pathology · 2019Review
- Intermediate Monocytes and Cytokine Production Associated With Severe Forms of Chagas Disease.Frontiers in immunology · 2019Article
- Review
- MyD88 activation in cardiomyocytes contributes to the heart immune response to acute Trypanosoma cruzi infection with no effect on local parasite control.PLoS neglected tropical diseases · 2018Article
- Biological factors that impinge on Chagas disease drug development.Parasitology · 2017Review
- Nitrotriazole-Based Compounds as Antichagasic Agents in a Long-TreatmentAntimicrobial agents and chemotherapy · 2017Article
- Chronic Chagas cardiomyopathy: a review of the main pathogenic mechanisms and the efficacy of aetiological treatment following the BENznidazole Evaluation for Interrupting Trypanosomiasis (BENEFIT) trial.Memorias do Instituto Oswaldo Cruz · 2017Article
- Trypanosoma cruzi High Mobility Group B (TcHMGB) can act as an inflammatory mediator on mammalian cells.PLoS neglected tropical diseases · 2017Article
- Chagas disease research and development: Is there light at the end of the tunnel?Computational and structural biotechnology journal · 2017Review
- Mechanisms of Infectivity and Evasion Derived from Microvesicles Cargo Produced byFrontiers in cellular and infection microbiology · 2016Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Over the past 20 years, the immune effector mechanisms involved in the control of Trypanosoma cruzi, as well as the receptors participating in parasite recognition by cells of the innate immune system, have been largely described. However, the main questions on the physiopathology of Chagas disease remain unanswered: "Why does the host immune system fail to provide sterile immunity?" and "Why do only a proportion of infected individuals develop chronic pathology?" In this review, we describe the mechanisms proposed to explain the inability of the immune system to eradicate the parasite and the elements that allow the development of chronic heart disease. Moreover, we discuss the possibility that the inability of infected cardiomyocytes to sense intracellular T. cruzi contributes to parasite persistence in the heart and the development of chronic pathology.
Indexed as
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What OpenQuestion holds
Registered trials
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.