Abstract
Traumatic brain injury (TBI) induced coagulopathy remains a significant clinical challenge,
with unmet needs for standardizing diagnosis and optimizing treatments. TBI-induced
coagulopathy is closely associated with poor outcomes in affected patients. Recent
studies have demonstrated that TBI induces coagulopathy, which is mechanistically
distinct from the deficient and dilutional coagulopathy found in patients with injuries
to the body/limbs and hemorrhagic shock. Multiple causal and disseminating factors
have been identified to cause TBI-induced coagulopathy. Among these are extracellular
mitochondria (exMTs) released from injured cerebral cells, endothelial cells, and
platelets. These circulating exMTs not only express potent procoagulant activity but
also promote inflammation, and could remain metabolically active to become a major
source of oxidative stress. They activate platelets and endothelial cells to propagate
TBI-induced coagulopathy and secondary tissue injury after primary traumatic impact.
In this review, we discuss recent advances in our understanding of the role of exMTs
in the development of TBI-induced coagulopathy.
Keywords
traumatic brain injury - mitochondria - extracellular vesicle - coagulopathy - inflammation
