Leviton Alan, Gressens Pierre, Wolkenhauer Olaf, Dammann Olaf
Neuroepidemiology Unit, Boston Children's Hospital Boston, MA, USA ; Department of Neurology, Harvard Medical School Boston, MA, USA.
Inserm, U1141 Paris, France ; Department of Perinatal Imaging and Health, Department of Division of Imaging Sciences and Biomedical Engineering, King's College London, King's Health Partners, St. Thomas' Hospital London, UK.
Front Syst Neurosci. 2015 Apr 14;9:58. doi: 10.3389/fnsys.2015.00058. eCollection 2015.
A systems approach to the study of brain damage in very preterm newborns has been lacking.
In this perspective piece, we offer encephalopathy of prematurity as an example of the complexity and interrelatedness of brain-damaging molecular processes that can be initiated inflammatory phenomena.
Using three transcription factors, nuclear factor-kappa B (NF-κB), Notch-1, and nuclear factor erythroid 2 related factor 2 (NRF2), we show the inter-connectedness of signaling pathways activated by some antecedents of encephalopathy of prematurity.
We hope that as biomarkers of exposures and processes leading to brain damage in the most immature newborns become more readily available, those who apply a systems approach to the study of neuroscience can be persuaded to study the pathogenesis of brain disorders in the very preterm newborn.
一直缺乏对极早产儿脑损伤进行研究的系统方法。
在这篇观点文章中，我们以早产儿脑病为例，说明可能引发炎症现象的脑损伤分子过程的复杂性和相互关联性。
我们使用三种转录因子，即核因子-κB（NF-κB）、Notch-1和核因子红细胞2相关因子2（NRF2），展示了由早产儿脑病的一些前驱因素激活的信号通路的相互联系。
我们希望，随着导致最不成熟新生儿脑损伤的暴露因素和过程的生物标志物变得更容易获得，那些采用系统方法研究神经科学的人能够被说服去研究极早产儿脑疾病的发病机制。
