THE NEUROENDOTHELIAL AXIS IN TRAUMATIC BRAIN INJURY: MECHANISMS OF MULTIORGAN DYSFUNCTION, NOVEL THERAPIES, AND FUTURE DIRECTIONS.
Shock
; 61(3): 346-359, 2024 Mar 01.
Article
in En
| MEDLINE
| ID: mdl-38517237
ABSTRACT
ABSTRACT Severe traumatic brain injury (TBI) often initiates a systemic inflammatory response syndrome, which can potentially culminate into multiorgan dysfunction. A central player in this cascade is endotheliopathy, caused by perturbations in homeostatic mechanisms governed by endothelial cells due to injury-induced coagulopathy, heightened sympathoadrenal response, complement activation, and proinflammatory cytokine release. Unique to TBI is the potential disruption of the blood-brain barrier, which may expose neuronal antigens to the peripheral immune system and permit neuroinflammatory mediators to enter systemic circulation, propagating endotheliopathy systemically. This review aims to provide comprehensive insights into the "neuroendothelial axis" underlying endothelial dysfunction after TBI, identify potential diagnostic and prognostic biomarkers, and explore therapeutic strategies targeting these interactions, with the ultimate goal of improving patient outcomes after severe TBI.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Endothelial Cells
/
Brain Injuries, Traumatic
Limits:
Humans
Language:
En
Journal:
Shock
Journal subject:
ANGIOLOGIA
/
CARDIOLOGIA
Year:
2024
Document type:
Article
Country of publication:
United States