cardiovascular system
N |
• under normal condition, mice exhibit normal cardiac function and mechanical properties
|
• after 2 weeks of treatment with angiotensin II, mice exhibit increased left ventricular end-diastolic diameter (LVEDD) compared with similarly treated wild-type mice
• however, a normal decrease in LVEDD a week after angiotensin II treatment is observed
|
• mice treated with angiotensin II or isoproterenol exhibit increased left ventricular dilation compared with similarly treated wild-type mice
|
• following treatment with angiotensin II or isoproterenol
|
• following treatment with angiotensin II or isoproterenol
|
• after 1 and 2 weeks of treatment with angiotensin II, mice exhibit decreased fractional shortening compared with similarly treated wild-type mice
• after treatment with isoproterenol, mice exhibit reduced ejection fraction and fractional shortening compared with similarly treated wild-type mice
|
homeostasis/metabolism
• mice treated with angiotensin II or isoproterenol exhibit left ventricular dilation, decreased fractional shortening, increased left ventricular end-diastolic diameter, and increased cardiac interstitial fibrosis compared with similarly treated wild-type mice
|
muscle
• following treatment with angiotensin II or isoproterenol
|
• after 1 and 2 weeks of treatment with angiotensin II, mice exhibit decreased fractional shortening compared with similarly treated wild-type mice
• after treatment with isoproterenol, mice exhibit reduced ejection fraction and fractional shortening compared with similarly treated wild-type mice
|
cellular
• following treatment with angiotensin II or isoproterenol
|
Mouse Models of Human Disease |
DO ID | OMIM ID(s) | Ref(s) | |
dilated cardiomyopathy 1G | DOID:0110430 |
OMIM:604145 |
J:152736 |