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. 2019 Feb 28;216(4):807–830. doi: 10.1084/jem.20171438

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© 2019 Mentrup et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 10. — The intramembrane proteases SPPL2a/b control the development of atherosclerosis. SPPL2a and SPPL2b maintain endothelial homeostasis by clearing LOX-1 NTFs generated by ADAM10 and in lysosomes, thereby releasing the LOX-1 ICD. In the absence of SPPL2a/b, LOX-1 NTFs accumulate, enhance oxLDL-induced signaling by full-length LOX-1, and activate MAP kinases in a ligand-independent manner. This promotes endothelial dysfunction and causes a pro-atherogenic and pro-fibrotic phenotype in SPPL2a/b double-deficient mice when challenged with hypercholesterolemia.