Blood-brain barrier pathophysiology in traumatic brain injury
By A. Chodobski, B. Zink, J. Szmydynger-Chodobska. Translational Stroke Research, 2011
610 citations recorded by the source corpus.
The blood–brain barrier (BBB) is formed by tightly connected cerebrovascular endothelial cells, but its normal function also depends on paracrine interactions between the brain endothelium and closely located glia. There is a growing consensus that brain injury, whether it is ischemic, hemorrhagic, or traumatic, leads to dysfunction of the BBB. Changes in BBB function observed after injury are thought to contribute to the loss of neural tissue and to affect the response to neuroprotective drugs. New discoveries suggest that considering the entire gliovascular unit, rather than the BBB alone, will expand our understanding of the cellular and molecular responses to traumatic brain injury (TBI). This review will address the BBB breakdown in TBI, the role of blood-borne factors in affecting the function of the gliovascular unit, changes in BBB permeability and post-traumatic edema formation, and the major pathophysiological factors associated with TBI that may contribute to post-traumatic dysfunction of the BBB. The key role of neuroinflammation and the possible effect of injury on transport mechanisms at the BBB will also be described. Finally, the potential role of the BBB as a target for therapeutic intervention through restoration of normal BBB function after injury and/or by harnessing the cerebrovascular endothelium to produce neurotrophic growth factors will be discussed.
Subfields: Molecular Biology, Neurology, Oncology
View Paper: https://www.semanticscholar.org/paper/2924ef8495d72ff778ab9322e669d1bc597cec63
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Citations in the corpus
- The Biology of Regeneration Failure and Success After Spinal Cord Injury. (2018, background): “Even as homeostasis and subsequent BSCB repair occurs, the basal lamina of the BSCB remains damaged, and in the absence of astrocytes in the lesion core, the junctions between endothelial cells fail to reform to their pre-injury state due to decreased expression of tight junction proteins such as cl”