Abstract
Brain edema remains a challenging obstacle in the management of acute liver failure (ALF). Cytotoxic mechanisms associated with brain edema have been well recognized, but evidence for vasogenic mechanisms in the pathogenesis of brain edema in ALF has been lacking. Recent reports have not only shown a role of matrix metalloproteinase-9 in the pathogenesis of brain edema in experimental ALF but have also found significant alterations in the tight junction elements including occludin and claudin-5, suggesting a vasogenic injury in the blood-brain barrier (BBB) integrity. This article reviews and explores the role of the paracellular tight junction proteins in the increased selective BBB permeability that leads to brain edema in ALF.
Original language | English (US) |
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Pages (from-to) | 676-683 |
Number of pages | 8 |
Journal | Neurochemistry International |
Volume | 60 |
Issue number | 7 |
DOIs | |
State | Published - Jun 2012 |
Keywords
- Acute liver failure
- Brain endothelial cell
- Paracellular permeability
- Tight junction
ASJC Scopus subject areas
- Cellular and Molecular Neuroscience
- Cell Biology