Hypercontractile Properties of Cardiac Muscle Fibers in a Knock-in Mouse Model of Cardiac Myosin-binding Protein-C
Why the study?
Does an N-terminal-shortened cardiac MyBP-C mutation alter contractile properties in a mouse model of familial hypertrophic cardiomyopathy?
Population
Knock-in mouse model carrying N-terminal-shortened cardiac Myosin-binding protein-C (MyBP-C)
Comparison
N-terminal-shortened cardiac MyBP-C mutation vs Wild-type mice
Design
Preclinical
Authors
Discussion
Loading...
Member takes
Implication
May promote hypercontractility in familial HCM; leaves open human translation from this animal model.
Structured PICO
Does an N-terminal-shortened cardiac MyBP-C mutation alter contractile properties in a mouse model of familial hypertrophic cardiomyopathy?
P
Population
Knock-in mouse model carrying N-terminal-shortened cardiac Myosin-binding protein-C (MyBP-C)
I
Intervention
N-terminal-shortened cardiac MyBP-C mutation (knock-in)
C
Comparator
Wild-type mice
O
Outcome
Ca(2+) sensitivity of force development in left ventricular fiberssurrogate
N-terminal mutations of cardiac MyBP-C may lead to a hypercontractile state by increasing calcium sensitivity of force development, providing insight into the pathophysiology of familial hypertrophic cardiomyopathy.
Cite This Study
Witt et al. (2001) studied this question.