Key result
Disruption of the iNOS gene improved beta-adrenergic inotropic responsiveness in transgenic mice with cytokine-induced cardiomyopathy but did not alter myocardial inflammation, hypertrophy, or survival.
Why the study?
Does disruption of the iNOS gene improve beta-adrenergic inotropic responsiveness and survival in mice with cytokine-induced cardiomyopathy?
Population
Transgenic mice with cardiac-specific overexpression of tumor necrosis factor-alpha
Comparison
Disruption of iNOS gene vs TG mice without iNOS disruption and age- and…
Design
Preclinical
Authors
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May enhance contractility without survival benefit in cytokine cardiomyopathy models; leaves open iNOS as a therapeutic target in human heart failure.
Does disruption of the iNOS gene improve beta-adrenergic inotropic responsiveness and survival in mice with cytokine-induced cardiomyopathy?
In a mouse model of cytokine-induced cardiomyopathy, iNOS disruption improves beta-adrenergic responsiveness but does not improve survival, indicating NO-independent mechanisms are key in heart failure development.
Funakoshi et al. (2002) studied Cytokine-induced cardiomyopathy. Disruption of iNOS gene vs. Transgenic mice without iNOS disruption and wild-type mice was evaluated on Beta-adrenergic inotropic responsiveness and survival. Disruption of the iNOS gene improved beta-adrenergic inotropic responsiveness in transgenic mice with cytokine-induced cardiomyopathy but did not alter myocardial inflammation, hypertrophy, or survival.
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