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Microglia, neurons, astrocytes, and endothelial cells can release proinflammatory cytokines and chemokines, modulating adhesion molecules and transmigration of activated immune cells into the brain parenchyma (Jickling et al., In addition, the increase in cellular levels of TNF- and IL-1 has been related to the decrease in occludin expression and ZO-1 and 2 in the hypoxic brain (Rochfort and Cummins, Oxidative stress has a critical role in BBB breakdown in different neurological conditions (Olmec and Ozyurt, Perinatal Programming of The NVU: Potential Epigenetic Mechanisms Adverse environmental conditions during development, such as prenatal hypoxia, can increase the risk of diseases in adulthood, such as vascular and parenchymal brain diseases (Berson et al., Hypoxic stress activates multiple epigenetic mechanisms in the fetal brain that increase the vulnerability for neurodevelopment disturbances in adult offspring (Ma et al., DNA methylation regulates the accessibility of DNA to the transcription machinery modifying the chromatin state