| First Author | Altamimi TR | Year | 2019 |
| Journal | J Mol Cell Cardiol | Volume | 127 |
| Pages | 223-231 | PubMed ID | 30615880 |
| Mgi Jnum | J:295150 | Mgi Id | MGI:6459692 |
| Doi | 10.1016/j.yjmcc.2018.12.019 | Citation | Altamimi TR, et al. (2019) Cardiac-specific deficiency of the mitochondrial calcium uniporter augments fatty acid oxidation and functional reserve. J Mol Cell Cardiol 127:223-231 |
| abstractText | The mitochondrial calcium uniporter (MCU) relays cytosolic Ca(2+) transients to the mitochondria. We examined whether energy metabolism was compromised in hearts from mice with a cardiac-specific deficiency of MCU subjected to an isoproterenol (ISO) challenge. Surprisingly, isolated working hearts from cardiac MCU-deficient mice showed higher cardiac work, both in the presence or absence of ISO. These hearts were not energy-starved, with ISO inducing a similar increase in glucose oxidation rates compared to control hearts, but a greater increase in fatty acid oxidation rates. This correlated with lower levels of the fatty acid oxidation inhibitor malonyl CoA, and to an increased stimulatory acetylation of its degrading enzyme malonyl CoA decarboxylase and of the fatty acid beta-oxidation enzyme beta-hydroxyacyl CoA dehydrogenase. We conclude that impaired mitochondrial Ca(2+) uptake does not compromise cardiac energetics due to a compensatory stimulation of fatty acid oxidation that provides a higher energy reserve during acute adrenergic stress. |
