Key result
Stable expression of triadin, independent of junctin expression, resulted in cardiac hypertrophy, prolonged basal relaxation, a depressed response to beta-adrenergic agonists, and altered Ca transients.
Population
Mice with heart-directed overexpression of triadin and junctin (JxT)
Design
Preclinical
Authors
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Triadin levels require precise regulation for normal contractility; leaves open its role in human heart failure phenotypes.
The maintenance of triadin expression is essential for normal sarcoplasmic reticulum calcium cycling and contractile function in the heart.
Kirchhefer et al. (2007) studied Cardiac hypertrophy and cellular Ca cycling. Heart-directed overexpression of triadin and junctin (JxT) vs. Wild-type/control mice (implied) was evaluated on Cardiac function, contractility, and Ca transient decay kinetics. Stable expression of triadin, independent of junctin expression, resulted in cardiac hypertrophy, prolonged basal relaxation, a depressed response to beta-adrenergic agonists, and altered Ca transients.
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