Key result
FKBP12 overexpression in mice cuts sodium current ~80% and drives sudden death.
Why the study?
The role of FKBP12 in regulating postnatal cardiac function and its impact on cardiac electrophysiology remain largely unknown.
Population
FKBP12 overexpressing transgenic and cardiomyocyte-restricted FKBP12 conditional knockout mice
Comparison
FKBP12 overexpression or knockout versus control mice/cardiomyocytes
Design
Preclinical experimental study with in vivo and in vitro electrophysiological analyses
Authors
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May implicate FKBP12 in murine arrhythmogenesis; hypothesis-generating for human cardiac electrophysiology and requires validation.
FKBP12 is a critical regulator of the cardiac voltage-gated sodium current, and its dysregulation may explain clinical arrhythmias associated with FK506 administration.
Maruyama et al. (2011) studied Cardiac electrophysiology and arrhythmia. FKBP12 overexpression or knockout vs. Wild-type/control mice was evaluated on Sudden death and cardiac voltage-gated sodium current I(Na). FKBP12 overexpression in mice led to a 38% incidence of sudden death and an approximately 80% reduction in peak density of the voltage-gated sodium current I(Na).
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