Elastin fragmentation in atherosclerotic mice leads to intraplaque neovascularization, plaque rupture, myocardial infarction, stroke, and sudden death

C. Van der Donckt,Jozef L. Van Herck,D. Schrijvers,G. Vanhoutte,M. Verhoye,I. Blockx,A. Van der Linden,D. Bauters,H. Lijnen,J. Sluimer,L. Roth,C. Van Hove,P. Fransen,M. Knaapen,Anne-Sophie Hervent,G. D. De Keulenaer,H. Bult,W. Martinet,A. Herman,G. D. De Meyer

Published 2014 in European Heart Journal

ABSTRACT

Our study underscores the importance of elastin fragmentation in the vessel wall as an accelerator of atherosclerosis with enhanced inflammation and increased neovascularization, thereby promoting the development of unstable plaques that eventually may rupture. The present mouse model offers the opportunity to further investigate the role of key factors involved in plaque destabilization and potential targets for therapeutic interventions.

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