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. 2019 Nov 9;116(14):2226–2238. doi: 10.1093/cvr/cvz303

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© The Author(s) 2019. Published by Oxford University Press on behalf of the European Society of Cardiology

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

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GPR109A gene deletion did not abrogate the protective effects of niacin against AAA formation in the CaCl₂ model. (A) AAA diameter (n = 6–15). (B) Representative histology; H&E, Mac-3 (macrophages), VVG (elastin fragmentation), MPO, and MCP-1. (C) Plasma MCP-1 levels (ELISA, n = 4–6). Data were analysed using one-way ANOVA followed by Bonferroni post hoc analysis. H&E, haematoxylin & eosin; L, lumen; Mac, macrophage; MCP-1, monocyte chemoattractant protein 1; MPO, myeloperoxidase; NA, nicotinic acid.