Key result
Replacing SERCA2a with SERCA2b in mice increases early mortality by ~20% and impairs cardiac contraction.
Why the study?
The requirement of muscle-specific SERCA2a isoform for normal cardiac function and development was unclear.
Population
Homozygous SERCA2a(-/-) mice with disrupted SERCA2a splicing mechanism
Comparison
Replacement of SERCA2a by SERCA2b isoform versus wild-type mice
Design
Gene targeting preclinical study in mice
Authors
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SERCA2a isoform specificity is essential in cardiac muscle; leaves open whether selective modulation offers therapeutic benefit in human HF.
The muscle-specific SERCA2a isoform is essential for normal cardiac development and the contraction-relaxation cycle, as its replacement by SERCA2b leads to hypertrophy and impaired cardiac function.
Heyen et al. (2001) studied Cardiac function and development. SERCA2a gene disruption (SERCA2a(-/-)) vs. Wild-type mice was evaluated on Cardiac function, mortality, and morphology. Replacement of the muscle-specific SERCA2a isoform by SERCA2b in mice caused a ~20% increase in early mortality, mild concentric cardiac hypertrophy, and impaired contraction-relaxation.
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