• Jessie W Ho, Zaiba Shafik Dawood, Meredith E Taylor, Marjorie R Liggett, Guang Jin, Dinesh Jaishankar, Satish N Nadig, Ankit Bharat, and Hasan B Alam.
• Department of Surgery, Division of Trauma Surgery and Critical Care, Feinberg School of Medicine, Northwestern University, Chicago, Illinois.
• Shock. 2024 Mar 1; 61 (3): 346359346-359.

AbstractSevere 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.Copyright © 2024 by the Shock Society.

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