Artículos de revistas
Perinatal asphyxia: CNS development and deficits with delayed onset
Fecha
2014Registro en:
Frontiers in Cellular Neuroscience, Volumen 8, Issue MAR, 2018,
16625102
10.3389/fnins.2014.00047
Autor
Herrera-Marschitz Muller, Mario
Neira-Pena, Tanya
Rojas-Mancilla, Edgardo
Espina Marchant, Pablo
Esmar, Daniela
Perez, Ronald
Muñoz, Valentina
Gutierrez-Hernandez, Manuel
Rivera, Benjamin
Simola, Nicola
Bustamante, Diego
Morales, Paola
Gebicke-Haerter, Peter J.
Institución
Resumen
Perinatal asphyxia constitutes a prototype of obstetric complications occurring when pulmonary oxygenation is delayed or interrupted. The primary insult relates to the duration of the period lacking oxygenation, leading to death if not re-established. Re-oxygenation leads to a secondary insult, related to a cascade of biochemical events required for restoring proper function. Perinatal asphyxia interferes with neonatal development, resulting in long-term deficits associated to mental and neurological diseases with delayed clinical onset, by mechanisms not yet clarified. In the experimental scenario, the effects observed long after perinatal asphyxia have been explained by overexpression of sentinel proteins, such as poly(ADP-ribose) polymerase-1 (PARP-1), competing for NAD+ during re-oxygenation, leading to the idea that sentinel protein inhibition constitutes a suitable therapeutic strategy. Asphyxia induces transcriptional activation of pro-inflammatory factors, in tandem with PARP-1