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The Molecular Mechanisms that Promote Edema After Intracerebral Hemorrhage

The Molecular Mechanisms that Promote Edema After Intracerebral Hemorrhage 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. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Translational Stroke Research Springer Journals

The Molecular Mechanisms that Promote Edema After Intracerebral Hemorrhage

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References (140)

Publisher
Springer Journals
Copyright
Copyright © 2012 by Springer Science+Business Media, LLC
Subject
Biomedicine; Neurosurgery; Cardiology; Vascular Surgery; Neurosciences; Neurology
ISSN
1868-4483
eISSN
1868-601X
DOI
10.1007/s12975-012-0162-0
pmid
24323861
Publisher site
See Article on Publisher Site

Abstract

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.

Journal

Translational Stroke ResearchSpringer Journals

Published: Apr 12, 2012

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