Abstract
The disruption of cerebral energy metabolism in relation to brain damage has been the subject of extensive research. However, the pyruvate dehydrogenase complex (PDHC), which is primarily characterized by poor cerebral energy metabolism following brain trauma, has received relatively little study in comparison to newborn hypoxic-ischemic brain injury. Mitochondrial PDHC, a multienzyme complex that functions as a crucial hub in energy metabolism and acts as a central metabolic node to mediate pyruvate oxidation after glycolysis and fuel the Krebs cycle to meet energy demands, has been reported to be one cause of energy metabolism dysfunction according to recent studies. Here we assess the potential mechanisms of neonatal hypoxic-ischemic brain injury-related brain dysfunction mediated by PDHC and further discuss the neuroprotective effects of therapeutic medicines that target PDHC activation. We also provide a summary of recent research on medicines that target PDHC in neonates with hypoxic-ischemic brain damage. Through an understanding of the mechanisms by which it is modulated and an investigation of the neuroprotective techniques available to activate brain PDHC and improve neonatal hypoxic-ischemic impairment, our review emphasizes the significance of PDHC impairment in neonatal hypoxic-ischemic brain injury.