Opportunities and Challenges in Chronic Chagas Cardiomyopathy

Mensah, George A.; Burns, Kristin M.; Peprah, Emmanuel; Sampson, Uchechukwu K.A.; Engelgau, Michael M.

doi:10.1016/j.gheart.2015.08.001

Cited by 7 publications

(2 citation statements)

References 59 publications

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“…Chagas disease, caused by the parasite Trypanosoma cruzi , is a potentially deadly disease endemic in Latin America [1, 2]. Approximately 30% of the infected patients develop cardiac problems, including Chronic Chagasic Cardiomyopathy (CCM), which is associated with high mortality [3,4]. The pathogenesis of CCM is not completely understood.…”

Section: Introductionmentioning

confidence: 99%

High fat diet aggravates cardiomyopathy in murine chronic Chagas disease

Lizardo¹,

Ayyappan²,

Cui

et al. 2019

Microbes and Infection

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Infection with Trypanosoma cruzi, the etiologic agent in Chagas disease, may result in heart disease. Over the last decades, Chagas disease endemic areas in Latin America have seen a dietary transition from the traditional regional diet to a Western style, fat rich diet. Previously, we demonstrated that during acute infection high fat diet (HFD) protects mice from the consequences of infection-induced myocardial damage through effects on adipogenesis in adipose tissue and reduced cardiac lipidopathy. However, the effect of HFD on the subsequent stages of infection - the indeterminate and chronic stages - has not been investigated. To address this gap in knowledge, we studied the effect of HFD during indeterminate and chronic stages of Chagas disease in the mouse model. We report, for the first time, the effect of HFD on myocardial inflammation, vasculopathy, and other types of dysfunction observed during chronic T. cruzi infection. Our results show that HFD perturbs lipid metabolism and induces oxidative stress to exacerbate late chronic Chagas disease cardiac pathology.

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Section: Introductionmentioning

confidence: 99%

High fat diet aggravates cardiomyopathy in murine chronic Chagas disease

Lizardo¹,

Ayyappan²,

Cui

et al. 2019

Microbes and Infection

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“…The potent innate and adaptive antibody and IFNγ-producing T cell response keeps parasitism in check, establishing a low-grade chronic infection. Most chronically infected patients (60%) remain healthy for life (the indeterminate/asymptomatic form) 11 , 12 . However, about 30% of chronically infected patients develop a life-threatening, symptomatic cardiac disease with inflammatory dilated cardiomyopathy up to 30 years after infection, Chronic Chagas disease Cardiomyopathy (CCC) 13 – 15 .…”

Section: Introductionmentioning

confidence: 99%

Integration of miRNA and gene expression profiles suggest a role for miRNAs in the pathobiological processes of acute Trypanosoma cruzi infection

Ferreira

Laugier

et al. 2017

Sci Rep

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Chagas disease, caused by the parasite Trypanosoma cruzi, is endemic in Latin America. Its acute phase is associated with high parasitism, myocarditis and profound myocardial gene expression changes. A chronic phase ensues where 30% develop severe heart lesions. Mouse models of T. cruzi infection have been used to study heart damage in Chagas disease. The aim of this study was to provide an interactome between miRNAs and their targetome in Chagas heart disease by integrating gene and microRNA expression profiling data from hearts of T. cruzi infected mice. Gene expression profiling revealed enrichment in biological processes and pathways associated with immune response and metabolism. Pathways, functional and upstream regulator analysis of the intersections between predicted targets of differentially expressed microRNAs and differentially expressed mRNAs revealed enrichment in biological processes and pathways such as IFNγ, TNFα, NF-kB signaling signatures, CTL-mediated apoptosis, mitochondrial dysfunction, and Nrf2-modulated antioxidative responses. We also observed enrichment in other key heart disease-related processes like myocarditis, fibrosis, hypertrophy and arrhythmia. Our correlation study suggests that miRNAs may be implicated in the pathophysiological processes taking place the hearts of acutely T. cruzi-infected mice.

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