mortality/aging
N |
• unexpectedly, homozygotes are born at normal Mendelian ratios and exhibit normal development and viability
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cardiovascular system
• in response to chronic beta-adrenergic stimulation, isoproterenol-treated mice appear to develop more cardiac fibrosis than isoproterenol-treated wild-type controls
• one of the isoproterenol-treated hearts showed a large area of fibrosis at the top of the right and left ventricular walls (>25% of myocardial area)
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• following isoproterenol treatment, mice fail to exhibit increased left ventricle fractional shortening (FS) and ejection fraction (EF), unlike isoproterenol-treated wild-type controls
• despite similar cardiac hypertrophic remodeling, isoproterenol-treated mice tend to exhibit lower left ventricle FS and EF than wild-type controls on day 13 of isoproterenol treatment
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• in response to chronic beta-adrenergic stimulation, isoproterenol-treated mice exhibit hypertrophic cardiac structural changes to a similar extent as in isoproterenol-treated wild-type controls but display a tend towards lower levels cardiac contractility (as measured by fractional shortening and ejection fraction) and increased cardiac fibrosis (as assessed by Massons trichrome staining)
• however, under normal physiological conditions, adult heart size and morphology is normal, with no significant alterations in cardiomyocyte organization and structure, levels of fibrosis or cardiac electrical activity
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homeostasis/metabolism
• in response to chronic beta-adrenergic stimulation, isoproterenol-treated mice exhibit hypertrophic cardiac structural changes to a similar extent as in isoproterenol-treated wild-type controls but display a tend towards lower levels cardiac contractility (as measured by fractional shortening and ejection fraction) and increased cardiac fibrosis (as assessed by Massons trichrome staining)
• however, under normal physiological conditions, adult heart size and morphology is normal, with no significant alterations in cardiomyocyte organization and structure, levels of fibrosis or cardiac electrical activity
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muscle
• following isoproterenol treatment, mice fail to exhibit increased left ventricle fractional shortening (FS) and ejection fraction (EF), unlike isoproterenol-treated wild-type controls
• despite similar cardiac hypertrophic remodeling, isoproterenol-treated mice tend to exhibit lower left ventricle FS and EF than wild-type controls on day 13 of isoproterenol treatment
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cellular
• in response to chronic beta-adrenergic stimulation, isoproterenol-treated mice appear to develop more cardiac fibrosis than isoproterenol-treated wild-type controls
• one of the isoproterenol-treated hearts showed a large area of fibrosis at the top of the right and left ventricular walls (>25% of myocardial area)
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