Journal article

Factor XII blockade inhibits aortic dilatation in angiotensin II-infused apolipoprotein E-deficient mice

Corey S Moran, Sai-Wang Seto, Erik Biros, Smriti M Krishna, Susan K Morton, Christoph Kleinschnitz, Con Panousis, Jonathan Golledge

CLINICAL SCIENCE | PORTLAND PRESS LTD | Published : 2020

Abstract

Abdominal aortic aneurysm (AAA) is an important cause of mortality in older adults. Chronic inflammation and excessive matrix remodelling are considered important in AAA pathogenesis. Kinins are bioactive peptides important in regulating inflammation. Stimulation of the kinin B2 receptor has been previously reported to promote AAA development and rupture in a mouse model. The endogenous B2 receptor agonist, bradykinin, is generated from the kallikrein-kinin system following activation of plasma kallikrein by Factor XII (FXII). In the current study whole-body FXII deletion, or neutralisation of activated FXII (FXIIa), inhibited expansion of the suprarenal aorta (SRA) of apolipoprotein E-defic..

View full abstract

Grants

Awarded by National Health and Medical Research Council


Awarded by Queensland Government


Awarded by National Health and Medical Research Council, Australia


Awarded by Queensland Government, Australia


Awarded by Deutsche Forschnungsgemeinschaft (German Research Foundation)


Funding Acknowledgements

This work was supported by the National Health and Medical Research Council [grant numbers 1098717, 1079369]; the Queensland Government [grant number SCRF]; in part by a Cardiac Health Institute Fellowship (to S.W.S.); a Practitioner Fellowship from the National Health and Medical Research Council, Australia [grant number 1117061 (to J.G.)]; a Senior Clinical Research Fellowship from the Queensland Government, Australia [grant number SCRF (to J.G.)]; the Deutsche Forschnungsgemeinschaft (German Research Foundation) [grant number SFB 688 (to C.K.)]; and employee of CSL Limited (Australia) (to C.P.). The funding bodies played no role in the production of this publication.