Journal
MOLECULAR NEUROBIOLOGY
Volume 28, Issue 3, Pages 229-244Publisher
SPRINGER
DOI: 10.1385/MN:28:3:229
Keywords
stroke; neuroprotection; neuromuscular unit; endothelial; blood-brain barrier
Categories
Funding
- NINDS NIH HHS [P50 NS 10828, R01 NS 40529, R02 NS 38731, R01 NS 37074] Funding Source: Medline
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS038731, P50NS010828, R01NS037074, R01NS040529] Funding Source: NIH RePORTER
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Intracerebral hemorrhagic transformation is a multifactorial phenomenon in which ischemic brain tissue converts into a hemorrhagic lesion with blood-vessel leakage, extravasation, and further brain injury. It has been estimated that up to 30-40% of all ischemic strokes undergo spontaneous hemorrhagic transformation, and this phenomenon may become even more prevalent with the increasing use of thrombolytic stroke therapy. An emerging conceptual model suggests that the loss of microvascular integrity and disruption of neurovascular homeostasis connects the experimental findings of blood-cell extravasation to brain injury after hemorrhage. In this short article, we examine mechanisms related to reperfusion injury and oxidative stress, leukocyte infiltration, vascular activation, and dysregulated extracellular proteolysis as potential triggers of hemorrhagic transformation. Perturbations in cell-cell and cell-matrix signaling within the hypothesized neurovascular unit may ultimately lead to neuroinflammation and apoptotic-like cell death in the parenchyma. Further investigations into the molecular mediators of hemorrhagic transformation may reveal new therapeutic targets for this clinically complex problem.
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