ArticleJournal of molecular and cellular cardiology2026
Mutation specific impairment of fatty acid and pyruvate oxidation in hypertrophic cardiomyopathy mouse models.
Article in Journal of molecular and cellular cardiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
background and hypothesisHypertrophic cardiomyopathy (HCM) is considered a metabolic disease, but it is unknown whether all sarcomeric protein gene mutations lead to similar derangements of cardiac energy metabolism. Our prior studies showing differences in mitochondrial function in mouse models led us to hypothesize that HCM mutations lead to allele-specific metabolic pathway remodeling. In order to test this hypothesis, we examined cardiac substrate utilization using a triple tracer approach that simultaneously assays fatty acid (FA), ketone, and glucose oxidation, in R403Q-MyHC and R92W-TnT perfused hearts at established disease stage.
methodsMouse hearts (14-16 weeks old) were Langendorff-perfused to steady state
resultsUsing a model of citric acid cycle (CAC) metabolism that equates MVO
conclusionCardiac metabolic flux measurements revealed an energy-deficient cardiac phenotype in R403Q-MyHC mutants, but not R92W-TnT mutants, reflecting allele-specific remodeling of cardiac energy metabolism. These results suggest that therapeutics aimed at downregulation of FA or carbohydrate metabolism may have mutation-specific effects.
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