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由肠道微生物群衍生的异酸通过抑制GSDME依赖性热死来缓解心房动

Ning Ding¹, Hao Wu¹, Yiming Hua¹

¹Department of Cardiovascular Medicine, First Affiliated Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi, China; Key Laboratory of Molecular Cardiology, Xi'an, Shaanxi, China; Key Laboratory of Environment and Genes Related to Diseases, Ministry of Education, Xi'an, Shaanxi, China.

Cell metabolism

|February 4, 2026

概括

肠道细菌Ruminococcus gnavus产生异酸,防止心房动 (AF) 和纤维化. 这种微生物代谢物通过抑制炎症信号和细胞死亡途径来保护心脏细胞.

科学领域:

微生物学微生物学
心脏病学心脏病学
代谢学代谢学代谢学

背景情况:

心房动 (AF) 是一种常见的心律失常,与肠道微生物失衡 (失调) 有关.
肠道微生物群影响AF和心房纤维化的具体机制尚未完全理解.

研究的目的:

调查肠道微生物群及其代谢物在心房的发病过程中的作用.
确定特定的微生物物种和参与AF发展和进展的代谢途径.

主要方法:

对人类临床队列和多种动物模型的综合分析.
鉴定和表征鲁米诺科克 (R. gnavus) 和其代谢产物.
研究了R. gnavus殖民和异酸 (IVA) 补充对AF易感性和心房纤维化的影响.
阐明了涉及G蛋白结合受体109A (GPR109A),介质素-6 (IL-6),信号转换器和转录3 (STAT3) 的激活器和气皮胺E (GSDME) 途径的分子机制.

主要成果:

鉴定出Ruminococcus gnavus是一种抑制AF和心房纤维化的肠道共生体.
这种细菌从食中的白中产生异酸 (IVA),从而降低了AF的易感性,并改善了心房重塑.
微生物组衍生的IVA在心房心肌细胞上激活GPR109A,抑制IL-6/STAT3信号传递和阻断GSDME介导的热.

结论:

肠道细菌R. gnavus及其代谢物IVA对心房动和相关纤维化起着保护作用.
微生物对白的代谢转化为IVA是预防AF发病和进展的关键因素.
针对R. gnavus-IVA-GPR109A轴是一个潜在的治疗策略来管理心房动.

关键词:

在 GPR109A 中使用.在GSDME中,GSDME是GSDME.在STAT3中,我们可以使用STAT3.心房动是心房动的一种.异酸是一种同酸.我们的微生物群.热致灭症是什么?

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