Pathology and new players in the pathogenesis of brain edema

被引:199
作者
Nag, Sukriti [1 ]
Manias, Janet L. [1 ]
Stewart, Duncan J. [2 ]
机构
[1] Univ Toronto, Dept Lab Med & Pathol, Banting Inst, Toronto, ON M5G IL5, Canada
[2] Univ Ottawa, Ottawa Hlth Res Inst, Ottawa, ON, Canada
关键词
Angiopoietins; Aquaporins; Blood-brain barrier; Brain edema; Caveolin-1; Claudin-5; Cold injury; Cytotoxic edema; JAM-A; Matrix metalloproteinases; Occludin; VEGF-A; VEGF-B; Vasogenic edema; ENDOTHELIAL GROWTH-FACTOR; FOCAL CEREBRAL-ISCHEMIA; VASCULAR-PERMEABILITY FACTOR; TIGHT JUNCTION STRANDS; PROTECTION FOLLOWING STROKE; RECEPTOR TYROSINE KINASE; B VEGF-B; BARRIER PERMEABILITY; MATRIX METALLOPROTEINASES; IN-VIVO;
D O I
10.1007/s00401-009-0541-0
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Brain edema continues to be a major cause of mortality after diverse types of brain pathologies such as major cerebral infarcts, hemorrhages, trauma, infections and tumors. The classification of edema into vasogenic, cytotoxic, hydrocephalic and osmotic has stood the test of time although it is recognized that in most clinical situations there is a combination of different types of edema during the course of the disease. Basic information about the types of edema is provided for better understanding of the expression pattern of some of the newer molecules implicated in the pathogenesis of brain edema. These molecules include the aquaporins, matrix metalloproteinases and growth factors such as vascular endothelial growth factors A and B and the angiopoietins. The potential of these agents in the treatment of edema is discussed. Since many molecules are involved in the pathogenesis of brain edema, effective treatment cannot be achieved by a single agent but will require the administration of a "magic bullet" containing a variety of agents released at different times during the course of edema in order to be successful.
引用
收藏
页码:197 / 217
页数:21
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