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Prog Neurobiol. 2013 Feb-Mar;101-102:65-82. doi: 10.1016/j.pneurobio.2012.11.004. Epub 2012 Dec 27.

Ischemic stroke and traumatic brain injury: the role of the kallikrein-kinin system.

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1
University Clinic of Würzburg, Department of Neurology, Würzburg, Germany. Albert_C2@klinik.uni-wuerzburg.de

Abstract

Acute ischemic stroke and traumatic brain injury are a major cause of mortality and morbidity. Due to the paucity of therapies, there is a pressing clinical demand for new treatment options. Successful therapeutic strategies for these conditions must target multiple pathophysiological mechanisms occurring at different stages of brain injury. In this respect, the kallikrein-kinin system is an ideal target linking key pathological hallmarks of ischemic and traumatic brain damage such as edema formation, inflammation, and thrombosis. In particular, the kinin receptors, plasma kallikrein, and coagulation factor XIIa are highly attractive candidates for pharmacological development, as kinin receptor antagonists or inhibitors of plasma kallikrein and coagulation factor XIIa are neuroprotective in animal models of stroke and traumatic brain injury. Nevertheless, conflicting preclinical evaluation as well as limited and inconclusive data from clinical trials suggest caution when transferring observations made in animals into the human situation. This review summarizes current evidence on the pathological significance of the kallikrein-kinin system during ischemic and traumatic brain damage, with a particular focus on experimental data derived from animal models. Experimental findings are also compared with human data if available, and potential therapeutic implications are discussed.

PMID:
23274649
DOI:
10.1016/j.pneurobio.2012.11.004
[Indexed for MEDLINE]
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