Key result
In genetic mouse models, loss of Mybphl accelerated the linear phase of relaxation in single atrial myofibrils and doubled cMyBP-C abundance in the atria.
Why the study?
The function of MyBP-HL and its relationship with cMyBP-C in atrial cardiomyocytes are unknown.
Population
Genetic mouse models and single atrial myofibrils
Comparison
Control vs Mybphl null single atrial myofibrils and cMyBP-C models
Design
Preclinical laboratory study
Authors
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Mybphl loss may accelerate atrial relaxation via cMyBP-C; leaves open its relevance to human atrial function or disease.
MyBP-HL regulates cMyBP-C abundance and alters the kinetics of sarcomere relaxation in atrial sarcomeres, providing insight into mechanisms of primary atrial myopathy.
Barefield et al. (2023) studied Primary atrial myopathy. Loss of MyBP-HL (Mybphl null) vs. Control was evaluated on Linear phase of relaxation in single atrial myofibrils. In genetic mouse models, loss of Mybphl accelerated the linear phase of relaxation in single atrial myofibrils and doubled cMyBP-C abundance in the atria.
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