菌可以通过激活肠道缺氧诱导因子2α信号来加速动脉样硬化
Xuemei Wang1, Shuang Zhou1, Xiaomin Hu2
1Department of Immunology, School of Basic Medical Sciences, NHC Key Laboratory of Medical Immunology, Medicine Innovation Center for Fundamental Research on Major Immunology-related Diseases, Peking University, Beijing 100191, China; Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University, Beijing 100191, China; Center for Obesity and Metabolic Disease Research, School of Basic Medical Sciences, Peking University, Beijing 100191, China.
肠道真菌失衡,特别是Candida albicans,与高胆固醇和动脉样硬化有关. 准的是肠道.
科学领域:
- 微生物学 微生物学
- 心血管科学 心血管科学
- 代谢性疾病 代谢性疾病
背景情况:
- 肠道微生物群在动脉样硬化中的作用已经确立,但肠道真菌的贡献仍然不清楚.
- 失脂症是动脉样硬化的一个危险因素,涉及到改变的脂质配置文件.
- 菌 (Candida albicans) 是一种常见的肠道真菌,具有潜在的致病作用.
研究的目的:
- 研究肠道真菌,特别是Candida albicans在动脉样硬化中的作用.
- 阐明将Candida albicans与动脉样硬化进展联系起来的分子机制.
- 探索针对已识别的途径的治疗潜力.
主要方法:
- 肠道真菌和血脂质在失脂症患者的分析.
- 一只老鼠动脉样的殖民化与Candida albicans.
- 功能增益和丧失研究,以调查低氧诱导因子2α (HIF-2α) - 胺路径.
- 在小鼠中使用HIF-2α抗剂PT2385.
主要成果:
- 肠道真菌失调,与增加的Candida albicans相关,与较高的总胆固醇和LDL-C在失脂症患者.
- 菌的殖民化加剧了小鼠中的动脉样硬化.
- 菌可以通过甲基甲胺激活肠道HIF-2α信号,增加胺合成并加速动脉样硬化.
- 在小鼠中,PT2385治疗降低了胺水平,并缓解了动脉样硬化.
结论:
- 肠道真菌,特别是Candida albicans,在动脉样硬化进展中发挥着重要作用.
- 肠道的HIF-2α-胺路径是Candida albicans对动脉样硬化影响的关键调解者.
- 准HIF-2α-胺通路为动脉样硬化症提供了潜在的治疗策略.
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