Key result
Myocardial overexpression of ANKRD1 in mice caused sinus venosus defects during development and progressive adult diastolic dysfunction with preserved ejection fraction.
Why the study?
The link between increased ANKRD1 levels and cardiac structural and functional disease was not understood.
Population
Gain of function ANKRD1 transgenic mouse model
Comparison
ANKRD1 myocardial overexpression vs controls
Design
Animal experimental study
Follow-up
Embryonic to adult life
Authors
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Hypothesis-generating for ANKRD1 in congenital and diastolic disease; leaves open human relevance pending translational studies.
Myocardial overexpression of ANKRD1 in a mouse model causes sinus venosus defects and progressive diastolic dysfunction, providing a mechanistic link to cardiac disease onset.
Piroddi et al. (2019) studied Cardiac structural and functional disease. Myocardial overexpression of ANKRD1 was evaluated on Cardiac structural and functional disease (sinus venosus defect, diastolic dysfunction). Myocardial overexpression of ANKRD1 in mice caused sinus venosus defects during development and progressive adult diastolic dysfunction with preserved ejection fraction.
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