mortality/aging
• lethality rates at 4 weeks after TAC are greater (53.3% vs. 30.7%) than in wild-type
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cardiovascular system
• mutants subjected to pressure overload induced by transversial aortic coarctation (TAC) develop abnormal cardiac remodeling that evolves into dilated cardiomyopathy and contractile dysfunction, with a typical pattern of eccentric hypertrophic remodeling instead of a concentric hypertrophy as in wild-type mice
• however, hypertrophic response is similar to wild-type after chronic administration of angiotensin II or phenylephrine (that is, in the absence of mechanical stress) at doses that do not increase blood pressure
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homeostasis/metabolism
• mutants subjected to pressure overload induced by transversial aortic coarctation (TAC) develop abnormal cardiac remodeling that evolves into dilated cardiomyopathy and contractile dysfunction, with a typical pattern of eccentric hypertrophic remodeling instead of a concentric hypertrophy as in wild-type mice
• however, hypertrophic response is similar to wild-type after chronic administration of angiotensin II or phenylephrine (that is, in the absence of mechanical stress) at doses that do not increase blood pressure
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