Mitochondrial dysfunction and oxidative stress in heart disease

Abstract

Heart disease: Signaling a halt to disease progression Heart disease progression could be tackled by targeting signaling molecules that cause oxidative stress. Jennifer Kwong at Emory University School of Medicine in Atlanta, USA, and co-workers reviewed research into the role of mitochondria and their associated signaling molecules in the development of heart disease. Mitochondria are a major source of reactive oxygen species (ROS), signaling molecules involved in muscle contraction and calcium transfer in the heart, but they also destroy ROS to maintain a balance. Disruption to this balance can lead to elevated ROS, causing DNA and cellular damage, triggering disease. Animal trials using drugs to target mitochondrial ROS show promise in limiting heart disease progression. Further research is needed to determine whether this approach will work in humans and which specific heart problems might benefit from such therapies.