ArticlePLoS neglected tropical diseases2013
Trypanosoma cruzi infection and endothelin-1 cooperatively activate pathogenic inflammatory pathways in cardiomyocytes.
Article in PLoS neglected tropical diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 39 citations in OpenAlex.
- Integrative Genomics Identifies Candidate Genes Underlying Trypanotolerance in Hybrid African Cattle.Evolutionary applications · 2026Article
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- Gut microbiota and atrial cardiomyopathy.Frontiers in cardiovascular medicine · 2025Review
- Immunomodulatory proteins from hookworms reduce cardiac inflammation and modulate regulatory responses in a mouse model of chronicFrontiers in parasitology · 2023Article
- The roles of COX-2 in protozoan infection.Frontiers in immunology · 2023Review
- Chagas Heart Disease: Beyond a Single Complication, from Asymptomatic Disease to Heart Failure.Journal of clinical medicine · 2022Review
- Aspirin-triggered resolvin D1 reduces parasitic cardiac load by decreasing inflammation in a murine model of early chronic Chagas disease.PLoS neglected tropical diseases · 2021Article
- Article
- Curcumin exerts anti-inflammatory and vasoprotective effects through amelioration of NFAT-dependent endothelin-1 production in mice with acute Chagas cardiomyopathy.Memorias do Instituto Oswaldo Cruz · 2018Article
- Mir-190b negatively contributes to the Trypanosoma cruzi-infected cell survival by repressing PTEN protein expression.Memorias do Instituto Oswaldo Cruz · 2015Article
- COX-2 rs20417 Polymorphism Is Associated with Stroke and White Matter Disease.Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association · 2015Article
- Role of cyclooxygenase-2 in Trypanosoma cruzi survival in the early stages of parasite host-cell interaction.Memorias do Instituto Oswaldo Cruz · 2015Article
- Cyclooxygenase-2 and Prostaglandin E2 Signaling through Prostaglandin Receptor EP-2 Favor the Development of Myocarditis during Acute Trypanosoma cruzi Infection.PLoS neglected tropical diseases · 2015Article
- The endothelin system has a significant role in the pathogenesis and progression of Mycobacterium tuberculosis infection.Infection and immunity · 2014Article
- Endothelin-1 and its role in the pathogenesis of infectious diseases.Life sciences · 2014Review
- Longistatin in tick saliva blocks advanced glycation end-product receptor activation.The Journal of clinical investigation · 2014Article
- Inhibition of cyclooxygenase-1 and cyclooxygenase-2 impairs Trypanosoma cruzi entry into cardiac cells and promotes differential modulation of the inflammatory response.Antimicrobial agents and chemotherapy · 2014Article
- In vitro and in vivo trypanocidal activity of H2bdtc-loaded solid lipid nanoparticles.PLoS neglected tropical diseases · 2014Article
- Role of FAK signaling in chagasic cardiac hypertrophy.The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious DiseasesArticle
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trypanosoma cruzi, the causative agent of Chagas' disease, induces multiple responses in the heart, a critical organ of infection and pathology in the host. Among diverse factors, eicosanoids and the vasoactive peptide endothelin-1 (ET-1) have been implicated in the pathogenesis of chronic chagasic cardiomyopathy. In the present study, we found that T. cruzi infection in mice induces myocardial gene expression of cyclooxygenase-2 (Cox2) and thromboxane synthase (Tbxas1) as well as endothelin-1 (Edn1) and atrial natriuretic peptide (Nppa). T. cruzi infection and ET-1 cooperatively activated the Ca(2+)/calcineurin (Cn)/nuclear factor of activated T cells (NFAT) signaling pathway in atrial myocytes, leading to COX-2 protein expression and increased eicosanoid (prostaglandins E(2) and F(2α), thromboxane A(2)) release. Moreover, T. cruzi infection of ET-1-stimulated cardiomyocytes resulted in significantly enhanced production of atrial natriuretic peptide (ANP), a prognostic marker for impairment in cardiac function of chagasic patients. Our findings support an important role for the Ca(2+)/Cn/NFAT cascade in T. cruzi-mediated myocardial production of inflammatory mediators and may help define novel therapeutic targets.
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