Mice lacking mitochondrial ferritin are more sensitive to doxorubicin-mediated cardiotoxicity.

ABSTRACT:

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Mitochondrial ferritin is a functional ferritin that localizes in the mitochondria. It is expressed in the testis, heart, brain, and cells with active respiratory activity. Its overexpression in cultured cells protected against oxidative damage and reduced cytosolic iron availability. However, no overt phenotype was described in mice with inactivation of the FtMt gene. Here, we used the doxorubicin model of cardiac injury in a novel strain of FtMt-null mice to investigate the antioxidant role of FtMt. These mice did not show any evident phenotype, but after acute treatment to doxorubicin, they showed enhanced mortality and altered heart morphology with fibril disorganization and severe mitochondrial damage. Signs of mitochondrial damage were present also in mock-treated

SUBMITTER: Maccarinelli F 

PROVIDER: S-EPMC4118045 | biostudies-literature | 2014 Aug

REPOSITORIES: biostudies-literature