Novel insights into the development of chagasic cardiomyopathy: Role of PI3Kinase/NO axis

Roman‐Campos, Danilo; Sales-Junior, Policarpo A.; Duarte, Hugo L.; Gomes, Enéas Ricardo de Morais; Lara, Aline; Campos, Paula Peixoto; Rocha, Nazareth N.; Resende, Rodrigo R.; Ferreira, Anderson J.; Guatimosim, Sílvia; Gazzinelli, Ricardo T.; Ropert, Catherine; Cruz, Jáder Santos

doi:10.1016/j.ijcard.2012.09.020

Cited by 21 publications

(50 citation statements)

References 36 publications

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“…9,22,23 In a previous study, we have shown that Colombian strain of T. cruzi causes marked collagen accumulation in the mice left ventricle. As shown in Figure 1A, using Picrosirius staining technique, we detected progressive collagen deposition in right ventricle of infected mice.…”

Section: Resultsmentioning

confidence: 94%

“…9 Thus, we used isolated right ventricular myocytes and patch-clamp technique to study the impact of Chagas disease on plasmatic membrane electrical properties.…”

Section: 3mentioning

confidence: 99%

“…The APR is a complex interplay between distinct ionic currents, notably the diversity of voltage-dependent K + currents. 9,25 To investigate the ionic basis to account for AP lengthening, we measured macroscopic outward and inward K + currents. Figure 6 shows the results for peak outward K + currents, which represent transient outward K + current component in cardiomyocytes (I to ).…”

Section: 3mentioning

confidence: 99%

“…2,3 Changes in heart function is connected to a set of cellular and molecular changes in cardiac tissue such as disrupted myofibrils, increased myocyte apoptosis, 4 collagen deposition, 5 oxidative stress, 6 altered cellular metabolism, 7 reduced cellular contractility, 8 and disturbance of electrical properties of the heart. 9,10 There are distinct hypotheses to explain the molecular mechanisms of altered electrical and contractility properties of the heart during Chagas disease. One of the most accepted explanations claims that chronic cytokine production in the heart is responsible for most of the observed cardiac alterations.…”

Section: Introductionmentioning

confidence: 99%

“…2,11 Clinical studies and animal models have shown that right and left ventricles are compromised during the time course of Chagas disease. 3,[8][9][10][12][13][14][15] It is already known that right ventricle function is dysregulated during Chagas disease, however, few studies have pointed out which molecular mechanisms are responsible for right ventricular myocyte dysfunction. 16,17 Herein, using a murine model of Chagas disease, we studied whether the changes in electrical properties of the isolated right ventricular myocyte in acute and chronic phases of the disease are correlated with tissue fibrosis, inflammatory infiltrate, and parasite persistence in the heart.…”

Section: Introductionmentioning

confidence: 99%

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Altered Cardiomyocyte Function and Trypanosoma cruzi Persistence in Chagas Disease

Cruz¹,

Santos‐Miranda²,

Sales-Junior³

et al. 2016

The American Society of Tropical Medicine and Hygiene

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Abstract. Chagas disease, caused by the triatominae Trypanosoma cruzi, is one of the leading causes of heart malfunctioning in Latin America. The cardiac phenotype is observed in 20-30% of infected people 10-40 years after their primary infection. The cardiac complications during Chagas disease range from cardiac arrhythmias to heart failure, with important involvement of the right ventricle. Interestingly, no studies have evaluated the electrical properties of right ventricle myocytes during Chagas disease and correlated them to parasite persistence. Taking advantage of a murine model of Chagas disease, we studied the histological and electrical properties of right ventricle in acute (30 days postinfection [dpi]) and chronic phases (90 dpi) of infected mice with the Colombian strain of T. cruzi and their correlation to parasite persistence. We observed an increase in collagen deposition and inflammatory infiltrate at both 30 and 90 dpi. Furthermore, using reverse transcriptase polymerase chain reaction, we detected parasites at 90 dpi in right and left ventricles. In addition, we observed action potential prolongation and reduced transient outward K + current and L-type Ca 2+ current at 30 and 90 dpi. Taking together, our results demonstrate that T. cruzi infection leads to important modifications in electrical properties associated with inflammatory infiltrate and parasite persistence in mice right ventricle, suggesting a causal role between inflammation, parasite persistence, and altered cardiomyocyte function in Chagas disease. Thus, arrhythmias observed in Chagas disease may be partially related to altered electrical function in right ventricle.

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Section: Resultsmentioning

confidence: 94%

“…9 Thus, we used isolated right ventricular myocytes and patch-clamp technique to study the impact of Chagas disease on plasmatic membrane electrical properties.…”

Section: 3mentioning

confidence: 99%

Section: 3mentioning

confidence: 99%