Key result
Truncated cardiac myosin binding protein-C markedly abbreviated the systolic elastance time course, peaking earlier (27.6 vs 47.8 ms) and reducing peak elastance compared to wild-type controls.
Why the study?
Does homozygous truncated cMyBP-C mutation alter the time course and magnitude of left ventricular systolic elastance in male mice?
Population
Intact hearts, trabeculae, and skinned fibers from wild-type and homozygous truncated cMyBP-C male mice, as…
Comparison
Homozygous truncated cMyBP-C mutation and… vs Wild-type (+/+) controls
Design
Preclinical
Authors
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Does not support clinical translation from mice; leaves open cMyBP-C truncation effects in human cardiomyopathy.
Does homozygous truncated cMyBP-C mutation alter the time course and magnitude of left ventricular systolic elastance in male mice?
Deficient incorporation of cMyBP-C leads to abnormal sarcomere shortening velocity and abbreviated muscle stiffening, providing mechanistic insights into the development of associated cardiac dysfunction.
Palmer et al. (2004) studied this question. Truncated cardiac myosin binding protein-C markedly abbreviated the systolic elastance time course, peaking earlier (27.6 vs 47.8 ms) and reducing peak elastance compared to wild-type controls.
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