sirolimus and Metabolism--Inborn-Errors

Cardiac hypertrophy is closely linked to impaired fatty acid oxidation, but the molecular basis of this link is unclear. Here, we investigated the loss of an obligate enzyme in mitochondrial long-chain fatty acid oxidation, carnitine palmitoyltransferase 2 (CPT2), on muscle and heart structure, function, and molecular signatures in a muscle- and heart-specific CPT2-deficient mouse (Cpt2

Topics: Acetylation; Animals; Atrial Remodeling; Cardiomegaly; Carnitine O-Palmitoyltransferase; Crosses, Genetic; Diet, Ketogenic; Drug Resistance; Enzyme Activation; Heart; Histone Deacetylase Inhibitors; Male; Mechanistic Target of Rapamycin Complex 1; Metabolism, Inborn Errors; Mice, Knockout; Mice, Transgenic; Mitochondria, Heart; Myocardium; Protein Kinase Inhibitors; Protein Processing, Post-Translational; Sirolimus; Specific Pathogen-Free Organisms; Survival Analysis