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. 2019 Jul 10;51(7):78. doi: 10.1038/s12276-019-0275-6

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 7 — In SMCs, the flagellin-TLR5-Nox4 axis stimulates H₂O₂ generation. Nox-mediated H₂O₂ production induces NF-kB activation, leading to IL-6 production for inflammation of SMCs and activating the Rac-JNK cascade for SMC migration. We have demonstrated that the flagellin-TLR5-Nox4 cascade is an important mediator in the formation of neointimal hyperplasia in atherosclerosis