TY  - JOUR
A1  - Albert-Weissenberger, Christiane
A1  - Mencl, Stine
A1  - Hopp, Sarah
A1  - Kleinschnitz, Christoph
A1  - Siren, Anna-Leena
T1  - Role of the kallikrein-kinin system in traumatic brain injury
T2  - Frontiers in Cellular Neuroscience
N2  - Traumatic brain injury (TBI) is a major cause of mortality and morbidity worldwide. Despite improvements in acute intensive care, there are currently no specific therapies to ameliorate the effects of TBI. Successful therapeutic strategies for TBI should target multiple pathophysiologic mechanisms that occur at different stages of brain injury. The kallikrein-kinin system is a promising therapeutic target for TBI as it mediates key pathologic events of traumatic brain damage, such as edema formation, inflammation, and thrombosis. Selective and specific kinin receptor antagonists and inhibitors of plasma kallikrein and coagulation factor XII have been developed, and have already shown therapeutic efficacy in animal models of stroke and TBI. However, conflicting preclinical evaluation, as well as limited and inconclusive data from clinical trials in TBI, suggests that caution should be taken before transferring observations made in animals to humans. This review summarizes current evidence on the pathologic significance of the kallikrein-kinin system during TBI in animal models and, where available, the experimental findings are compared with human data.
KW  - bradykinin
KW  - factor XII
KW  - kallikrein–kinin system
KW  - kinin receptor
KW  - traumatic brain injury
Y1  - 2014
UR  - https://opus.bibliothek.uni-wuerzburg.de/frontdoor/index/index/docId/11822
UR  - https://nbn-resolving.org/urn:nbn:de:bvb:20-opus-118226
SN  - 1662-5102
VL  - 8
ER  -