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肠道微生物群衍生的氧化三甲胺抑制SIRT1，以调节SM22α介导的平滑肌细胞炎症并促进动脉粥样硬化进展。

Gut microbiota-derived trimethylamine-N-oxide inhibits SIRT1 to regulate SM22α-mediated smooth muscle cell inflammation and promote atherosclerosis progression.

作者信息

Yin Yajuan, Wei Mei, Jiang Xiufang, Liu Mei, Shi Xiaocui, Zhang Xiao, Wang Le, Liu Gang, Zheng Mingqi, Ma Fangfang

机构信息

Department of Cardiology The First Hospital of Hebei Medical University Shijiazhuang Hebei China.

Department of Medical Affaires The First Hospital of Hebei Medical University Shijiazhuang Hebei China.

出版信息

J Cell Commun Signal. 2025 Jun 6;19(2):e70021. doi: 10.1002/ccs3.70021. eCollection 2025 Jun.

DOI:10.1002/ccs3.70021
PMID:40486531
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12143968/
Abstract

Atherosclerosis (AS) is a prevalent cardiovascular disease, and emerging evidence highlights the critical role of gut microbiota in its development. Trimethylamine-N-oxide (TMAO), a metabolite derived from gut microbiota, is thought to promote AS progression by regulating smooth muscle protein 22-alpha (SM22α)-mediated inflammation in vascular smooth muscle cells. This study aims to explore the molecular mechanisms of TMAO in AS through multi-omics analysis, particularly its effects on SIRT1 inhibition and SM22α modulation. 16S ribosomal RNA sequencing revealed an altered gut microbiota composition in AS mice, characterized by increased Bacteroides and decreased Firmicutes. Metabolomics analysis indicated elevated levels of TMAO in AS mice. Transcriptomic data and cell experiments further confirmed that TMAO promotes AS by regulating SM22α-mediated inflammation via SIRT1 regulation. These findings suggest that TMAO accelerates progression through the SIRT1 and SM22α-related pathways, offering novel therapeutic targets for AS intervention.

摘要

动脉粥样硬化（AS）是一种常见的心血管疾病，新出现的证据突出了肠道微生物群在其发展中的关键作用。氧化三甲胺（TMAO）是一种源自肠道微生物群的代谢产物，被认为通过调节血管平滑肌细胞中平滑肌蛋白22-α（SM22α）介导的炎症来促进AS进展。本研究旨在通过多组学分析探索TMAO在AS中的分子机制，特别是其对SIRT1抑制和SM22α调节的影响。16S核糖体RNA测序显示AS小鼠的肠道微生物群组成发生改变，其特征是拟杆菌增加而厚壁菌减少。代谢组学分析表明AS小鼠中TMAO水平升高。转录组数据和细胞实验进一步证实，TMAO通过SIRT1调节来调节SM22α介导的炎症，从而促进AS。这些发现表明，TMAO通过SIRT1和SM22α相关途径加速进展，为AS干预提供了新的治疗靶点。

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