Loss of cardiac carnitine palmitoyltransferase 2 in mice initiates deleterious hypertrophic cardiac remodeling independent of fibrosis that is impervious to hypertrophy attenuators.
Loss of cardiac CPT2 leads to hypertrophic remodeling that is resistant to typical attenuators, highlighting the role of mitochondrial metabolism in cardiac growth.
hearts 2.3-fold compared with littermate control mice fed a ketogenic diet, yet it did not improve cardiac hypertrophy. Together, these results suggest that a shift away from mitochondrial fatty acid oxidation initiates deleterious hypertrophic cardiac remodeling independent of fibrosis. The data also indicate that CPT2-deficient hearts are impervious to hypertrophy attenuators, that mitochondrial metabolism regulates cardiac acetylation, and that signals derived from alterations in mitochondrial metabolism are the key mediators of cardiac hypertrophic growth.
Pereyra et al. (Sat,) conducted a other in Cardiac hypertrophy. Ketogenic diet vs. Littermate control mice was evaluated on Cardiac hypertrophy. Loss of cardiac carnitine palmitoyltransferase 2 in mice initiates deleterious hypertrophic cardiac remodeling independent of fibrosis that is impervious to hypertrophy attenuators.