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| elevated oxidative stress in MYPBC3-mutated dilated cardiomyopathy (DCM) mice, which may exacerbate the development of heart failure  | |
mechanism leading to cardiac dilation in homozygous Mybpc3(-/-) mice is primarily myocyte hyperplasia, and mechanism leading to hypertrophic cardiomyopathy in heterozygous Mybpc3(+/-) individuals is myocyte hypertrophy (increased cell size) |
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autophagy is impaired in Mybpc3-targeted knockin mice, and activation of autophagy ameliorated the cardiac disease phenotype in this mouse model |