Key result
Triadin 1 overexpression in transgenic mice triggered time-dependent alterations in SR protein expression, Ca(2+) homeostasis, and contractility, including a 110% increase in atrial weight at 18 weeks.
Population
Transgenic mice overexpressing canine cardiac triadin 1 under control of the alpha-myosin heavy chain promoter
Design
Preclinical
Follow-up
18 weeks
Authors
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Triadin 1 modulation should not yet change clinical practice; leaves open its role in human atrial remodeling pending translational studies.
Triadin 1 overexpression in transgenic mice demonstrates an inhibitory function of triadin 1 on SR-Ca(2+) release in vivo, leading to altered contractility and atrial hypertrophy.
Kirchhefer et al. (2002) studied Cardiac function and SR-Ca(2+) release. Triadin 1 overexpression was evaluated on Time-dependent expression of SR proteins and contractility in atria. Triadin 1 overexpression in transgenic mice triggered time-dependent alterations in SR protein expression, Ca(2+) homeostasis, and contractility, including a 110% increase in atrial weight at 18 weeks.
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