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PLoS One. 2013;8(1):e53577. doi: 10.1371/journal.pone.0053577. Epub 2013 Jan 4.

Cardiomyocyte specific deletion of Crif1 causes mitochondrial cardiomyopathy in mice.

Author information

1
Department of Biological Sciences, Seoul National University, Gwanak-gu, Seoul, Republic of Korea.

Abstract

Mitochondria are key organelles dedicated to energy production. Crif1, which interacts with the large subunit of the mitochondrial ribosome, is indispensable for the mitochondrial translation and membrane insertion of respiratory subunits. To explore the physiological function of Crif1 in the heart, Crif1(f/f) mice were crossed with Myh6-cre/Esr1 transgenic mice, which harbor cardiomyocyte-specific Cre activity in a tamoxifen-dependent manner. The tamoxifen injections were given at six weeks postnatal, and the mutant mice survived only five months due to hypertrophic heart failure. In the mutant cardiac muscles, mitochondrial mass dramatically increased, while the inner structure was altered with lack of cristae. Mutant cardiac muscles showed decreased rates of oxygen consumption and ATP production, suggesting that Crif1 plays a critical role in the maintenance of both mitochondrial structure and respiration in cardiac muscles.

PMID:
23308255
PMCID:
PMC3537664
DOI:
10.1371/journal.pone.0053577
[Indexed for MEDLINE]
Free PMC Article

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