TY - JOUR
T1 - The Molecular Mechanisms that Promote Edema After Intracerebral Hemorrhage
AU - Bodmer, Daniel
AU - Vaughan, Kerry A.
AU - Zacharia, Brad E.
AU - Hickman, Zachary L.
AU - Connolly, E. Sander
N1 - Funding Information:
Acknowledgments We apologize to authors whose work could not be cited due to space limitations. E.S.C. is supported by National Institutes of Health funding.
PY - 2012/7
Y1 - 2012/7
N2 - Intracerebral hemorrhage (ICH) is a devastating type of stroke with no effective therapies. Clinical advances in ICH treatment are limited by an incomplete understanding of the molecular mechanisms responsible for secondary injury and poor outcome. Increasing evidence suggests that cerebral edema is a major contributor to secondary injury and poor outcome in ICH. ICH activates specific signaling pathways that promote edema and damage neuronal tissue. By increasing our understanding of these pathways, we may be able to target them pharmaceutically to reduce edema in ICH patients. In this review, we focus on three major signaling pathways that promote edema after ICH: (1) the coagulation cascade and thrombin, (2) the inflammatory response and matrix metalloproteinases, and (3) the complement cascade and hemoglobin toxicity. We will describe the experimental evidence that confirms these pathways promote edema in ICH, discuss potential targets for new therapies, and comment on important directions for future research.
AB - Intracerebral hemorrhage (ICH) is a devastating type of stroke with no effective therapies. Clinical advances in ICH treatment are limited by an incomplete understanding of the molecular mechanisms responsible for secondary injury and poor outcome. Increasing evidence suggests that cerebral edema is a major contributor to secondary injury and poor outcome in ICH. ICH activates specific signaling pathways that promote edema and damage neuronal tissue. By increasing our understanding of these pathways, we may be able to target them pharmaceutically to reduce edema in ICH patients. In this review, we focus on three major signaling pathways that promote edema after ICH: (1) the coagulation cascade and thrombin, (2) the inflammatory response and matrix metalloproteinases, and (3) the complement cascade and hemoglobin toxicity. We will describe the experimental evidence that confirms these pathways promote edema in ICH, discuss potential targets for new therapies, and comment on important directions for future research.
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U2 - 10.1007/s12975-012-0162-0
DO - 10.1007/s12975-012-0162-0
M3 - Review article
C2 - 24323861
AN - SCOPUS:84862267134
SN - 1868-4483
VL - 3
SP - 52
EP - 61
JO - Translational Stroke Research
JF - Translational Stroke Research
IS - SUPPL. 1
ER -