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Vascular smooth muscle cells (VSMCs) can transdifferentiate into macrophage-like cells in the context of sustained inflammatory injury, which drives vascular hyperplasia and atherosclerotic complications. Using single-cell RNA sequencing, we identify that macrophage-like VSMCs are the key cell population in mouse neointimal hyperplasia. Sex-determining region Y (SRY)-related HMG-box gene 10 (Sox10) upregulation is associated with macrophage-like VSMC accumulation and pyroptosis in vitro and in the neointimal hyperplasia of mice. Tumor necrosis factor α (TNF-α)-induced Sox10 lactylation in a phosphorylation-dependent manner by PI3K/AKT signaling drives transcriptional programs of VSMC transdifferentiation, contributing to pyroptosis. The regulator of G protein signaling 5 (RGS5) interacts with AKT and blocks PI3K/AKT signaling and Sox10 phosphorylation at S24. Sox10 silencing mitigates vascular inflammation and forestalls neointimal hyperplasia in RGS5 knockout mice. Collectively, this study shows that Sox10 is a regulator of vascular inflammation and a potential control point in inflammation-related vascular disease. Copyright © 2023 The Author(s). Published by Elsevier Inc. All rights reserved.

Citation

Xin Xu, Dan-Dan Zhang, Peng Kong, Ya-Kun Gao, Xiao-Fu Huang, Yu Song, Wen-Di Zhang, Rui-Juan Guo, Chang-Lin Li, Bo-Wen Chen, Yue Sun, Yong-Bo Zhao, Fang-Yue Jia, Xu Wang, Fan Zhang, Mei Han. Sox10 escalates vascular inflammation by mediating vascular smooth muscle cell transdifferentiation and pyroptosis in neointimal hyperplasia. Cell reports. 2023 Aug 29;42(8):112869

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PMID: 37481722

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