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A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
A mouse model of dilated-type cardiomyopathy due to coxsackievirus B3
Abstract:
Myocardial scarring was induced in 111 mice (group 3) inoculated at 14 days of age with coxsackievirus B3 and forced to swim for 30 min daily during the initial nine days of infection. The animals were observed until age 15 months. Control animals included mice infected but not forced to swim (group 2), neither infected nor forced to swim (group 1), and not infected but forced to swim (group 4). The cumulative mortality was 45% among mice in group 3 but was significantly lower in the control animals. At 15 months, mice in group 3 showed heavy deposits of calcium in the injured myocardium, atrial hypertrophy with thrombi, and myocardial fiber disintegration with replacement by fibrous scar. Mononuclear infiltration was no longer present. Pathologic changes were concentrated in the left ventricle, interventricular septum, and atrioventricular junction. Titers of type-specific neutralizing antibodies had declined to one-fifth the level present at one month. These findings represent a model of dilated-type cardiomyopathy.
Insights
This study developed a mouse model for dilated-type cardiomyopathy by infecting young mice with coxsackievirus B3 and inducing stress. The model showed significant mortality and cardiac pathology, mimicking human heart disease.
Area of Science:
- Cardiology
- Virology
- Pathology
Background:
- Coxsackievirus B3 infection is a known cause of viral myocarditis.
- Stress factors can exacerbate viral-induced heart damage.
Purpose of the Study:
- To establish a novel mouse model for dilated-type cardiomyopathy.
- To investigate the long-term effects of coxsackievirus B3 infection combined with physical stress on cardiac health.
Main Methods:
- Induction of myocardial scarring in 111 mice (group 3) via coxsackievirus B3 inoculation and forced swimming.
- Observation of animals until 15 months of age.
- Comparison with control groups: infected without swimming, neither infected nor swimming, and swimming without infection.
Main Results:
- Group 3 mice exhibited 45% cumulative mortality, significantly higher than controls.
- At 15 months, group 3 mice displayed myocardial calcification, atrial hypertrophy with thrombi, and fibrosis.
- Pathologic changes were localized to the left ventricle, interventricular septum, and atrioventricular junction.
Conclusions:
- The described method successfully models dilated-type cardiomyopathy in mice.
- This model is characterized by chronic cardiac damage, fibrosis, and increased mortality.
- Findings suggest a link between viral infection, stress, and the progression to dilated cardiomyopathy.
