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• W1966187802 startingPage "263" @default.
• W1966187802 abstract "Genetic analysis of hypertrophic cardiomyopathy (HCM), a mendelian form of cardiac hypertrophy, indicates that the primary defect is in sarcomeric function. However, the initial proposal that depressed myocardial contraction leads to a ‘compensatory’ hypertrophy has proven inconsistent with laboratory and clinical evidence. Drawing on observations of mutant contractile protein function, together with mouse models and clinical studies, we propose that sarcomeric HCM mutations lead to inefficient ATP utilization. The suggestion that energy depletion underlies HCM is supported by the HCM-like phenotype found with mutations in a variety of metabolic genes. A central role for compromised energetics would also help explain the unresolved clinical observations of delayed onset and asymmetrical hypertrophy in HCM, and would have implications for therapy in HCM and, potentially, in more-common forms of cardiac hypertrophy and failure." @default.
• W1966187802 created "2016-06-24" @default.
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• W1966187802 date "2003-05-01" @default.
• W1966187802 modified "2023-10-04" @default.
• W1966187802 title "Hypertrophic cardiomyopathy:a paradigm for myocardial energy depletion" @default.
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• W1966187802 doi "https://doi.org/10.1016/s0168-9525(03)00081-7" @default.
• W1966187802 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/12711218" @default.
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