HCM
Here we tested whether proteasome inhibition could also reverse the disease phenotype in a genetically-modified mouse model of hypertrophic cardiomyopathy (HCM), which carries a mutation in Mybpc3, encoding the myofilament protein cardiac myosin-binding protein C. At 7 weeks of age, homozygous mutant mice (KI) have 39% higher left ventricular mass-to-body-weight ratio and 29% lower fractional area shortening (FAS) than wild-type (WT) mice.
Here we tested whether proteasome inhibition could also reverse the disease phenotype in a genetically-modified mouse model of <span class="disease" id="25566086-3-127-154">hypertrophic cardiomyopathy</span> (<span class="disease" id="25566086-3-156-159">HCM</span>), which carries a mutation in <span class="gene" id="25566086-3-190-196">Mybpc3</span>, encoding the myofilament protein cardiac myosin-binding protein C. At 7 weeks of age, homozygous mutant mice (KI) have 39% higher left ventricular mass-to-body-weight ratio and 29% lower fractional area shortening (FAS) than wild-type (WT) mice.