Genetic deletion of ASIC3 impacts left ventricular remodeling and autonomic nervous system responses, suggesting a potential target for heart failure therapies.
Key Points
ASIC3-/- mice exhibited less left ventricular dilation after myocardial infarction, indicating altered cardiac remodeling.
Measurements showed increased stroke volume in ASIC3-/- mice compared to wild type, highlighting the impact of ASIC3 on cardiac function.
Baroreceptor reflex sensitivity was lower in ASIC3-/- mice after myocardial infarction, correlated with changes in left ventricular mass.
This research suggests ASIC3 may serve as a therapeutic target in heart failure by influencing neurohormonal responses.