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由间歇性禁食增加的来自Akkermansia muciniphila的新型蛋白B2URF3缓解了血管化

Shi-Yu Zeng^1,2, Jiang-Hua Liu³, Ying-Ying Xiang¹

¹Department of Metabolism and Endocrinology, The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, 421001, Hunan, China.

Journal of nanobiotechnology

|January 8, 2026

概括

隔日间歇性禁食 (IF1:1) 通过增强肠道细菌,特别是Akkermansia muciniphila,减少小鼠的血管化. 这种效应涉及携带蛋白B2URF3的Akk衍生的细胞外囊泡,提供潜在的治疗点.

科学领域:

心血管研究研究心血管研究
微生物组科学微生物组科学
代谢性疾病代谢性疾病

背景情况:

血管化 (VC) 显著增加心血管疾病的风险,有效治疗方法有限.
人们越来越认识到肠道微生物组在包括血管功能在内的全身健康中的作用.

研究的目的:

为了研究间歇性禁食 (IF) 方案在预防维生素D诱导的VC的有效性.
阐明肠道微生物群及其衍生的细胞外囊泡 (EVs) 在介导IF对VC的保护作用中的作用.
为了确定特定的分子机制和潜在的生物标志物,涉及到肠-血管轴.

主要方法:

使用小鼠模型的维生素D诱导VC来比较交替日 (IF1:1) 和 5:2 IF疗法.
评估了IF对肠道微生物群组成的影响,重点是Akkermansia muciniphila (Akk).
在体外和体内的血管光滑肌细胞 (VSMCs) 中研究了Akk衍生的EVs (Akk-EVs) 的功能.
进行蛋白质组分析以确定Akk-EVs和Akk中的关键蛋白质,并验证了与宿主蛋白质的相互作用.
分析了冠状动脉化患者的和血清样本,以与临床观察结果相关联.

主要成果:

在老鼠中,交替一日间断食 (IF1:1) 显著减弱了维生素D诱导的VC,而5:2 IF疗法是无效的.
IF1:1的保护作用取决于肠道微生物群,特别是Akermansia muciniphila (Akk) 的丰富.
阿克克-EV被VSMC内部化,抑制骨质分化和化.
在Akk-EVs和Akk中非常丰富的蛋白B2URF3被确定为一个关键的调解者,与ALDH1B1相互作用以抑制VSMC骨质变异.
在冠状动脉化患者中观察到便中减少的Akk丰度和较低的血清B2URF3水平.

结论:

隔天间歇性禁食建立了一条肠血管轴,减轻了血管化.
在这种保护机制中,Akkermansia muciniphila及其衍生的细胞外囊泡 (Akk-EVs) 起着至关重要的作用.
Akk-EV蛋白B2URF3是抑制VSMC骨质分化的关键介质,是血管化的潜在治疗标和生物标记物.

关键词:

阿克尔曼西亚木类动物生活.细胞外囊泡中的细胞外囊泡.肠 - 血管轴肠 - 血管轴断断续续的禁食是一种禁食.血管化是因为血管化.

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