ArticlePLoS neglected tropical diseases2017
Cardiomyocyte oxidants production may signal to T. cruzi intracellular development.
Article in PLoS neglected tropical diseases, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Anti-inflammatory and antioxidant therapies for chagasic myocarditis: a systematic review.Parasitology · 2020Pooled it
- Differential antioxidant enzyme profiles reveal early molecular signatures of virulence inFrontiers in cellular and infection microbiology · 2025Article
- Heart function enhancement by an Nrf2-activating antioxidant in acute Y-strain Chagas disease, but not in chronic Colombian or Y-strain.PLoS neglected tropical diseases · 2024Article
- Differential Regulation of L-Arginine Metabolism through NOS2 and Arginases during Infection withPathogens (Basel, Switzerland) · 2024Article
- In vitro characterization of Trypanosoma cruzi infection dynamics in skeletal and cardiac myotubes models suggests a potential cell-to-cell transmission in mediating cardiac pathology.PLoS neglected tropical diseases · 2024Article
- Differential cardiomyocyte transcriptomic remodeling during in vitro Trypanosoma cruzi infection using laboratory strains provides implications on pathogenic host responses.Tropical medicine and health · 2023Article
- Cardiomyocyte infection byFrontiers in cellular and infection microbiology · 2023Article
- Characterization and functional analysis of the proteins Prohibitin 1 and 2 in Trypanosoma cruzi.PLoS neglected tropical diseases · 2021Article
- Cyclophilin 19 secreted in the host cell cytosol by Trypanosoma cruzi promotes ROS production required for parasite growth.Cellular microbiology · 2021Article
- DNA damage and oxidative stress in human cells infected by Trypanosoma cruzi.PLoS pathogens · 2021Article
- Impairment of Multiple Mitochondrial Energy Metabolism Pathways in the Heart of Chagas Disease Cardiomyopathy Patients.Frontiers in immunology · 2021Article
- The Oxidative Stress and Chronic Inflammatory Process in Chagas Disease: Role of Exosomes and Contributing Genetic Factors.Oxidative medicine and cellular longevity · 2021Review
- Transcriptional Studies onFrontiers in cellular and infection microbiology · 2021Review
- Advances in Cardiotoxicity Induced by Altered Mitochondrial Dynamics and Mitophagy.Frontiers in cardiovascular medicine · 2021Review
- Priming Astrocytes With HIV-Induced Reactive Oxygen Species Enhances TheirFrontiers in microbiology · 2020Article
- Neuronal Parasitism, Early Myenteric Neurons Depopulation and Continuous Axonal Networking Damage as Underlying Mechanisms of the Experimental Intestinal Chagas' Disease.Frontiers in cellular and infection microbiology · 2020Article
- Differential Modulation of Mouse Heart Gene Expression by Infection With TwoFrontiers in genetics · 2020Article
- Direct and Indirect Inhibition Effects of Resveratrol againstAntimicrobial agents and chemotherapy · 2019Article
- Pyridinecarboxylic Acid Derivative Stimulates Pro-Angiogenic Mediators by PI3K/AKT/mTOR and Inhibits Reactive Nitrogen and Oxygen Species and NF-κB Activation Through a PPARγ-Dependent Pathway inFrontiers in immunology · 2019Article
- Anti-parasitic effect of vitamin C alone and in combination with benznidazole against Trypanosoma cruzi.PLoS neglected tropical diseases · 2018Article
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8 authors.
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Abstract
Chagas disease, caused by the protozoan parasite Trypanosoma cruzi, presents a variable clinical course, varying from asymptomatic to serious debilitating pathologies with cardiac, digestive or cardio-digestive impairment. Previous studies using two clonal T. cruzi populations, Col1.7G2 (T. cruzi I) and JG (T. cruzi II) demonstrated that there was a differential tissue distribution of these parasites during infection in BALB/c mice, with predominance of JG in the heart. To date little is known about the mechanisms that determine this tissue selection. Upon infection, host cells respond producing several factors, such as reactive oxygen species (ROS), cytokines, among others. Herein and in agreement with previous data from the literature we show that JG presents a higher intracellular multiplication rate when compared to Col1.7G2. We also showed that upon infection cardiomyocytes in culture may increase the production of oxidative species and its levels are higher in cultures infected with JG, which expresses lower levels of antioxidant enzymes. Interestingly, inhibition of oxidative stress severely interferes with the intracellular multiplication rate of JG. Additionally, upon H2O2-treatment increase in intracellular Ca2+ and oxidants were observed only in JG epimastigotes. Data presented herein suggests that JG and Col1.7G2 may sense extracellular oxidants in a distinct manner, which would then interfere differently with their intracellular development in cardiomyocytes.
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