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. 2018 Jan 24;7(3):e007004. doi: 10.1161/JAHA.117.007004

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© 2018 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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Fibrotic and inflammatory changes of the myocardium resulting from left ventricular pressure overload are decreased in mice treated with recombinant human a disintegrin‐like metalloproteinase with thrombospondin motif type 1 member 13 (rhADAMTS13). A, Immunohistochemical staining for intercellular adhesion molecule‐1 (ICAM‐1), a marker for endothelial activation, demonstrated stronger staining in coronary vessel endothelium and endocardium of vehicle‐treated mice compared with rhADAMTS13‐treated mice 28 days after ascending aortic constriction (AAC), suggesting an anti‐inflammatory effect of rhADAMTS13. B, Collagen deposition in the heart 28 days after AAC was significantly lower in rhADAMTS13‐ than vehicle‐treated mice (sham, n=4; vehicle, n=5; rhADAMTS13, n=7).