Loss of integrity: Impairment of the blood-brain barrier in heavy metal-associated ischemic stroke

被引：21
作者：
Kim J.-H. [1 ]
Byun H.-M. [1 ]
Chung E.-C. [1 ]
Chung H.-Y. [2 ]
Bae O.-N. [1 ,3 ]
机构：
[1] College of Pharmacy, Hanyang University, Gyeonggi-do
[2] Department of Biotechnology and Bioinformatics, Korea University, Sejong City
[3] Institute of Pharmaceutical Science and Technology, Hanyang University, Gyeonggi-do
来源：
Toxicological Research | 2013年 / 29卷 / 3期
关键词：
Blood-brain barrier; Heavy metals; Ischemic stroke; Neurovascular unit; Tight junction;
D O I：
10.5487/TR.2013.29.3.157
中图分类号：
学科分类号：
摘要：
Although stroke is one of the leading causes of death and disability worldwide, preventive or therapeutic options are still limited. Therefore, a better understanding of the pathophysiological characteristics of this life-threatening disease is urgently needed. The incidence and prevalence of ischemic stroke are increased by exposure to certain types of xenobiotics, including heavy metals, suggesting the possible toxicological contribution of these compounds to the onset or aggravation of stroke. Among the potential targets, we have focused on alterations to cerebral endothelial cells (CECs), which play important roles in maintaining the functional integrity of brain tissue.
引用
收藏
页码：157 / 164
页数：7
相关论文
共 72 条
[1]  
O'Donnell M.J., Xavier D., Liu L., Zhang H., Chin S.L., Rao-Melacini P., Rangarajan S., Islam S., Pais P., Mcqueen M.J., Mondo C., Damasceno A., Lopez-Jaramillo P., Hankey G.J., Dans A.L., Yusoff K., Truelsen T., Diener H.C., Sacco R.L., Ryglewicz D., Czlonkowska A., Weimar C., Wang X., Yusuf S., Investigators I., Risk factors for ischaemic and intracerebral haemorrhagic stroke in 22 countries (the INTERSTROKE study): a case-control study, Lancet, 376, pp. 112-123, (2010)
[2]  
Fisher M., New approaches to neuroprotective drug development, Stroke, 42, (2011)
[3]  
Savitz S.I., Fisher M., Future of neuroprotection for acute stroke: in the aftermath of the SAINT trials, Ann. Neurol., 61, pp. 396-402, (2007)
[4]  
Roger V.L., Go A.S., Lloyd-Jones D.M., Benjamin E.J., Berry J.D., Borden W.B., Bravata D.M., Dai S., Ford E.S., Fox C.S., Fullerton H.J., Gillespie C., Hailpern S.M., Heit J.A., Howard V.J., Kissela B.M., Kittner S.J., Lackland D.T., Lichtman J.H., Lisabeth L.D., Makuc D.M., Marcus G.M., Marelli A., Matchar D.B., Moy C.S., Mozaffarian D., Mussolino M.E., Nichol G., Paynter N.P., Soliman E.Z., Sorlie P.D., Sotoodehnia N., Turan T.N., Virani S.S., Wong N.D., Woo D., Turner M.B., Heart disease and
[5]  
Lo E.H., Dalkara T., Moskowitz M.A., Mechanisms, challenges and opportunities in stroke, Nat. Rev. Neurosci., 4, pp. 399-415, (2003)
[6]  
Dirnagl U., Iadecola C., Moskowitz M.A., Patho-biology of ischaemic stroke: an integrated view, Trends Neurosci., 22, pp. 391-397, (1999)
[7]  
Macdonald J.F., Xiong Z.G., Jackson M.F., Paradox of Ca2+ signaling, cell death and stroke, Trends Neurosci., 29, pp. 75-81, (2006)
[8]  
Graham S.H., Chen J., Programmed cell death in cerebral ischemia, J. Cereb. Blood Flow Metab., 21, pp. 99-109, (2001)
[9]  
Lo E.H., Moskowitz M.A., Jacobs T.P., Exciting, radical, suicidal: how brain cells die after stroke, Stroke, 36, pp. 189-192, (2005)
[10]  
Green A.R., Pharmacological approaches to acute ischaemic stroke: reperfusion certainly, neuroprotection possibly, Br. J. Pharmacol., 153 Suppl, 1, (2008)
12345678