ENA0000GenomicsComputational Biology, Target Sciences, GlaxoSmithKlinehttps://www.ebi.ac.uk/ena/browser/view/PRJNA376517Mus musculusSkeletal muscle has an impressive ability to repair itself after a damaging insult and this response is essential to the process of muscle adaptation. In conditions such as muscular dystrophy and the sarcopenia of old age, repair is compromised leading to fibrosis and fatty tissue accumulation. Hypoxia-inducible factors (HIFs) are highly conserved regulators of gene transcription under conditions of low oxygen tension and HIF target genes such as EPO and VEGF have been associated with muscle protection and repair. We sought to interrogate the importance of HIF activation to skeletal muscle repair through the use of prolyl hydroxylase inhibitors (PHI) that stabilize HIF and activate target gene transcription in a mouse eccentric exercise limb damage model. We used microarrays to detail the global effects of prolyl hydroxylase inhibitors (PHI) in a mouse eccentric exercise limb damage model. Overall design: Normal C57Bl6/NJ mice were housed individually and fed standard chow and water ad libitum. Right hind limbs were injured while left hind limbs were used as control. Animals were treated either with PHI or vehicle. Gastrocnemius samples were collected after 3 hrs, 6hrs, and 9hrs, respectively.ENAResearch Related Injuries, Injury, Proline, Wound, Injury and Wounds, Prolyl Hydroxylase, Physical, wound, Physical Traumas, 2-Oxoglutarate 4-Dioxygenase, injury, skeletal muscle, Injuries and Wounds, Prolyl 4-Hydroxylase, Injuries, trauma, Injuries., somatic muscle, Wounds, traumatic injury, Wounds and Injury, Prolyl, Traumas, Trauma, Proline Hydroxylase, Research-Related Injuries, Peptidyl Prolyl Hydroxylase, Physical Trauma, Research-Related Injury, Hydroxylases, Research-Related, striated muscle, skeletal muscle systemmouse, mouse <Mus musculus>, house mouse.00.00.00.00.00.0falseMus musculusHIF Prolyl Hydroxylase Inhibition Protects Skeletal Muscle from Contraction-Induced Injury2022-05-122017-08-24PRJNA376517GSE9524410090