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. 2021 Jan 15;11:1552. doi: 10.1038/s41598-021-81282-9

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© The Author(s) 2021

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Proposed pathogenesis of vascular occlusion in MMD. Under normal conditions, the intact peri-endothelial matrix protects against vascular shear stress by relaxing VSMCs through the enhanced production of nitric oxide. In MMD, decreased production of CS leads to changes in the peri-endothelial matrix, including decreased HA, which makes the endothelium susceptible to vascular shear stress. EPCs infiltrate through the damaged endothelium, with HAS2 and COX2 subsequently induced in EPCs by shear stress or cytokines. The accumulation of HA in the intima, produced by the infiltrated EPCs, results in eccentric thickening of the intima and narrowing of the vascular lumen, which further increases shear stress.