期刊
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY
卷 2013, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2013/297512
关键词
-
类别
资金
- Sectorial Operational Programme Human Resources Development (SOPHRD)
- European Social Fund
- Romanian Government [POSDRU/89/1.5/S/64109]
- Executive Unit for Financing Higher Education, Research, Development and Innovation, Romania (UEFISCDI)
- National Research Council (CNCS) Grant, Romania [PN-II-ID-PCE-2012-4-0566/2013]
As fundamental research advances, it is becoming increasingly clear that a clinically expressed disease implies a mixture of intertwining molecular disturbances. Oxidative stress is one of such pathogenic pathways involved in virtually all central nervous system pathologies, infectious, inflammatory, or degenerative in nature. Since brain homeostasis largely depends on integrity of blood-brain barrier (BBB), many studies focused lately on BBB alteration in a wide spectrum of brain diseases. The proper two-way molecular transfer through BBB depends on several factors, including the functional status of its tight junction (TJ) complexes of proteins sealing neighbour endothelial cells. Although there is abundant experimental work showing that oxidative stress associates BBB permeability alteration, less is known about its implications, at molecular level, in TJ protein expression or TJ-related cell signalling. In this paper, oxidative stress is presented as a common pathway for different brain pathogenic mechanisms which lead to BBB dysregulation. We revise here oxidative-induced molecular mechanisms of BBB disruption and TJ protein expression alteration, in relation to ageing and neurodegeneration.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据