Exercise-induced mitochondrial translocation of p53 repairs mitochondrial DNA mutations

ABSTRACT: Exercise is a fundamental component of human health that is associated with greater life expectancy and reduced risk of chronic diseases. While the beneficial effects of endurance exercise on human health are well established, the molecular mechanisms responsible for these observations remain unclear. Endurance exercise reduces the accumulation of mitochondrial DNA (mtDNA) mutations, alleviates multisystem pathology, and increases the lifespan of the mtDNA mutator mouse model of aging, in which the proof-reading capacity of mitochondrial polymerase gamma (POLG1) is deficient. Clearly, exercise recruited a POLG1-independent mtDNA repair pathway to induce these adaptations, a novel finding as POLG1 is canonically considered to be the sole mtDNA repair enzyme. Here we investigate the identity

ORGANISM(S): Mus musculus

SUBMITTER: James Flynn 

PROVIDER: E-GEOD-75869 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress