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肠道细菌 Akkermansia muciniphila 抑制腹腔大动脉动脉瘤的进展

Xin He¹, Yu Liu^2,3,4, Haiyang Zhou^2,3,4

¹Department of Anesthesiology, Xiangya Hospital, Central South University, Changsha, China.

Antioxidants & redox signaling

|November 15, 2025

概括

阿克尔曼西亚菌 (Akkermansia muciniphila,Akk) 通过减少炎症和细胞死亡,在治疗腹腔大动脉动脉瘤 (AAA) 中表现有前途. 阿克激活AMPK以抑制铁亡,为AAA提供了一个潜在的治疗策略.

科学领域:

血管生物学血管生物学
微生物组研究微生物组研究
分子医学是分子医学.

背景情况:

腹腔大动脉瘤 (AAA) 是一种危及生命的疾病,治疗选择有限.
肠道微生物组,特别是阿克尔曼西亚菌 (Akk) 在AAA病变发生过程中的作用尚未完全理解.
研究分子机制对于开发新的治疗策略至关重要.

研究的目的:

阐明Akkermansia muciniphila (Akk) 在腹腔大动脉动脉瘤 (AAA) 中发挥治疗作用的分子机制.
探索Akk,中性粒细胞外细胞陷 (NETs),高流动性组盒1 (HMGB1) 和VSMC中的铁亡之间的相互作用.
确定关键的信号通路,如AMPK,参与Akk对AAA的保护作用.

主要方法:

16S rRNA测序用于分析肠道微生物组成.
转录组测序以识别对Akk治疗的反应中的分子变化.
在体内AAA模型和体内细胞研究使用血管光滑肌细胞 (VSMC).
评估细胞外基质降解,NET形成和铁亡.

主要成果:

艾克克治疗显著降低了AAA的发展和细胞外矩阵降解.
阿克克抑制了HMGB1诱导的NET形成,这是AAA进展的关键驱动力.
Akk激活了AMP激活蛋白激酶 (AMPK),以抑制VSMC铁,一种涉及AAA的细胞死亡形式.
HMGB1加剧了铁亡,而Akk对AMPK的激活逆转了这种效应.

结论:

阿克尔曼西亚 (Akk) 通过抑制HMGB1介导的NET形成和通过AMPK激活减少VSMC铁.
这些发现突出了一个新的治疗途径,涉及AAA中的肠道微生物群和细胞代谢.
阿克克是开发用于腹腔大动脉动脉瘤的创新疗法的有希望的候选人.

关键词:

16S rRNA 测序的测序方法由AMP激活的蛋白质激酶激活的蛋白质激酶.阿克尔曼西亚的木偶生活.腹部大动脉动脉瘤腹部大动脉动脉瘤铁性化 (ferroptosis) 是一种高流动性组第1框高流动性组第1框中性粒细胞外细胞陷

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