Liam A. Hurst

Learn More
BACKGROUND Mitochondrial DNA (mtDNA) damage occurs in both circulating cells and the vessel wall in human atherosclerosis. However, it is unclear whether mtDNA damage directly promotes atherogenesis or is a consequence of tissue damage, which cell types are involved, and whether its effects are mediated only through reactive oxygen species. METHODS AND(More)
Genetic diagnosis of inherited metabolic disease is conventionally achieved through syndrome recognition and targeted gene sequencing, but many patients receive no specific diagnosis. Next-generation sequencing allied to capture of expressed sequences from genomic DNA now offers a powerful new diagnostic approach. Barriers to routine diagnostic use include(More)
Heterozygous germ-line mutations in the bone morphogenetic protein type-II receptor (BMPR-II) gene underlie heritable pulmonary arterial hypertension (HPAH). Although inflammation promotes PAH, the mechanisms by which inflammation and BMPR-II dysfunction conspire to cause disease remain unknown. Here we identify that tumour necrosis factor-α (TNFα)(More)
We welcome the opportunity to respond to comments from Drs Stocker and Maghzal on our article. Increased reactive oxygen species (ROS) occur in human atherosclerosis in many cell types, and multiple experimental manipulations (predominantly in mice) suggest that ROS promote atherosclerosis. Because mitochondria are an important source of ROS that could be(More)
Background -Pulmonary arterial hypertension (PAH) is characterized by abnormal growth and enhanced glycolysis of pulmonary artery endothelial cells (PAECs). However, the mechanisms underlying alterations in energy production have not been identified. Methods -Here, we examined the miRNA and proteomic profiles of blood outgrowth endothelial cells (BOECs)(More)
  • 1