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Alterations of Blood-Brain Barrier and Associated Factors in Acute Liver Failure
Author(s) -
Wei Cui,
Cui-Ming Sun,
Pei Liu
Publication year - 2013
Publication title -
gastroenterology research and practice
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.622
H-Index - 45
eISSN - 1687-630X
pISSN - 1687-6121
DOI - 10.1155/2013/841707
Subject(s) - occludin , tight junction , medicine , blood–brain barrier , claudin , paracellular transport , edema , vascular permeability , barrier function , pathology , permeability (electromagnetism) , central nervous system , microbiology and biotechnology , biology , biochemistry , membrane
Brain edema in acute liver failure (ALF) remains lethal. Cytotoxic mechanisms associated with brain edema have been well recognized, but the role of vasogenic mechanisms of brain edema has not been explored. Intact tight junctions (TJs) between brain capillary endothelial cells are critical for normal BBB function. Recent reports found significant alterations in the tight junction elements including occludin and claudin-5, suggesting a vasogenic injury in the blood-brain barrier (BBB) integrity. However, the role of TJ in ALF has not been completely understood. This paper reviews the role of the paracellular tight junction in the increased selective BBB permeability that leads to brain edema in ALF and furthermore explores the effect of systemic inflammatory cytokines on the tight junction dysfunction.

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