Dear Colleagues,

Neonatal hypoxic-ischemic brain damage (HIBD), induced by a hypoxic event and the interruption of cerebral blood supply to the brain, is one of the most common causes of neonatal death and long-term neurodevelopmental impairments. These impairments include mental retardation, epilepsy, cerebral palsy and visual deficits, as well as cognitive and motor dysfunctions later in life. Thus far, the only clinically recommended and established intervention is moderate hypothermia, which involves cooling down newborns within the therapeutic time window of 72 h after the hypoxic-ischemic event. However, nearly half of the patients still suffer from major neurological problems. Moreover, the risk of thrombocytopenia and cardiac arrhythmias during treatment is increased. Therefore, there is an urgent need to explore new effective therapies to further reduce the rate and severity of neurodevelopmental disabilities resulting from neonatal HIBD. 

Oxidative stress is caused by the overproduction of reactive oxygen species (ROS) and diminished cellular antioxidant defenses, which plays an important role in pathogenesis and progression. Following hypoxic-ischemic attacks, the cellular macromolecules will be damaged by excess ROS. These derivatives induce a complex interplay of multiple pathways (e.g., inflammation, apoptosis, autophagy, and necrosis) which finally lead to brain injury. As the immature brain has high oxygen consumption and an underdeveloped antioxidant system, neonatal brains are more susceptible to oxidative stress.

This special issue aims to focus on the mechanism of oxidative stress in neonatal HIBD and provide new insights on potential therapies. We welcome basic and clinical studies as well as reviews in all areas pertinent to this topic.

Jia-Wei Min
Guest Editor