Role of the Kallikrein-kinin System in Traumatic Brain Injury

Overview

Journal Front Cell Neurosci

Specialty Cell Biology

Date 2014 Nov 19

PMID 25404891

Citations 10

Authors

Christiane Albert-Weissenberger

Stine Mencl

Sarah Hopp

Christoph Kleinschnitz

Anna-Leena Siren

Affiliations

Soon will be listed here.

Abstract

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.

Citing Articles

Emerging trends and focus of research on the relationship between traumatic brain injury and gut microbiota: a visualized study.

Du Q, Li Q, Liao G, Li J, Ye P, Zhang Q Front Microbiol. 2023; 14:1278438.

PMID: 38029105 PMC: 10654752. DOI: 10.3389/fmicb.2023.1278438.

Modulation of Neuro-Inflammatory Signals in Microglia by Plasma Prekallikrein and Neuronal Cell Debris.

Jaffa A, Jaffa M, Moussa M, Ahmed I, Karam M, Aldeen K Front Pharmacol. 2021; 12:743059.

PMID: 34867349 PMC: 8636058. DOI: 10.3389/fphar.2021.743059.

Association of Angiotensin-Converting Enzyme Inhibitors with Increased Mortality Among Patients with Isolated Severe Traumatic Brain Injury.

Catapano J, Chapman A, Dull M, Abbatematteo J, Horner L, Godzik J Neurocrit Care. 2019; 31(3):507-513.

PMID: 31187434 DOI: 10.1007/s12028-019-00755-y.

Human tissue kallikrein in the treatment of acute ischemic stroke.

Alexander-Curtis M, Pauls R, Chao J, Volpi J, Bath P, Verdoorn T Ther Adv Neurol Disord. 2019; 12:1756286418821918.

PMID: 30719079 PMC: 6348491. DOI: 10.1177/1756286418821918.

Alleviation of secondary brain injury, posttraumatic inflammation, and brain edema formation by inhibition of factor XIIa.

Hopp S, Nolte M, Stetter C, Kleinschnitz C, Siren A, Albert-Weissenberger C J Neuroinflammation. 2017; 14(1):39.

PMID: 28219400 PMC: 5319055. DOI: 10.1186/s12974-017-0815-8.

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