2020
DOI: 10.1016/j.bjid.2020.08.007
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Role of FAK signaling in chagasic cardiac hypertrophy

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Cited by 9 publications
(6 citation statements)
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“…The cardiac indices of the nitazoxanide-treated animals were at a midpoint between those of the BNZ and W-O/T groups, therefore affirming that the progression to cardiomegaly was partially decreased in comparison with not receiving treatment. These results were consistent with the important pathological outcome of chronic chagasic cardiomyopathy, since multiple factors such as severe myocarditis and fibrosis cause a hemodynamic overload of the heart, which represents a compensatory mechanism that leads to myocardial hypertrophy [ 41 ]. On the other hand, it has been reported that nitazoxanide induces myocardial injury by activating the oxidative stress response [ 42 ].…”
Section: Discussionsupporting
confidence: 82%
“…The cardiac indices of the nitazoxanide-treated animals were at a midpoint between those of the BNZ and W-O/T groups, therefore affirming that the progression to cardiomegaly was partially decreased in comparison with not receiving treatment. These results were consistent with the important pathological outcome of chronic chagasic cardiomyopathy, since multiple factors such as severe myocarditis and fibrosis cause a hemodynamic overload of the heart, which represents a compensatory mechanism that leads to myocardial hypertrophy [ 41 ]. On the other hand, it has been reported that nitazoxanide induces myocardial injury by activating the oxidative stress response [ 42 ].…”
Section: Discussionsupporting
confidence: 82%
“…cruzi had not been studied. Herein, AT-RvD1 was shown to reduce both the cross-sectional area of cardiomyocytes and the transcription of hypertrophy markers such as ANP and BNP, which have been associated with different stages and severity of CCC [ 63 , 64 ]. Furthermore, during T .…”
Section: Discussionmentioning
confidence: 99%
“…To the best of our knowledge, until now, the effect of AT-RvD1 on hypertrophy produced by infection with T. cruzi had not been studied. Herein, AT-RvD1 was shown to reduce both the cross-sectional area of cardiomyocytes and the transcription of hypertrophy markers such as ANP and BNP, which have been associated with different stages and severity of CCC [63,64]. Furthermore, during T. cruzi infection, the participation of endothelin-1, cardiotrophin-1, and cytokines such as TNFα and IL-1β has been previously highlighted as pro-hypertrophic [65].…”
Section: At-rvd1 Decreases the Inflammatory Process In Early Chronic CDmentioning
confidence: 91%
“…To the best of our knowledge, until now, the effect of AT-RvD1 on hypertrophy produced by infection with T. cruzi had not been studied. Herein, AT-RvD1 was shown to reduce both the crosssectional area of cardiomyocytes and the transcription of hypertrophy markers such as ANP and BNP, which have been associated with different stages and severity of CCC [54,55]. Furthermore, during T. cruzi infection, the participation of endothelin-1, cardiotrophin-1, and cytokines such as TNFα and IL-1β has been previously highlighted as pro-hypertrophic [56].…”
Section: At-rvd1 Decreases the Inflammatory Process In Chronic CDmentioning
confidence: 91%