贝尼-科吉的病理生理机制 霍莱斯特-帮助或 puberulic 酸诱导的损伤
Yuta Sekiguchi1, Makiko Mori1, Haruka Maruyama1,2
1Department of Nephrology, Graduate School of Medical and Dental Sciences, Institute of Science Tokyo, Tokyo, Japan.
Kidney international reports
|February 24, 2026
概括
红酵母补充剂中含有毒的 puberulic 酸会通过破坏管细胞中的线粒体引起损伤. 这一发现阐明了与这些补充剂相关的广泛健康问题背后的机制.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 毒理学 毒理学 毒理学
- 分子生物学分子生物学
背景情况:
- 在2024年3月,由于与特定的红酵母大米补充剂相关的损伤,日本出现了重大健康危机.
- 超过2600人寻求医疗护理,其中许多人经历了估计的球过率持续下降.
- 在受污染的补充剂中发现了 puberulic 酸,但其在观察到的毒性中的作用尚不清楚.
研究的目的:
- 调查有毒红酵母大米补充剂和 puberulic 酸对功能的影响.
- 阐明相关毒性背后的细胞和分子机制.
主要方法:
- 使用多种模型:人类脏活检样本,人类初级脏近壁管状上皮细胞 (hRPTECs),人类脏器官和小鼠.
- 进行了RNA测序 (RNA-seq),细胞外流量分析和组织学检查.
- 进行了体外实验,以评估细胞毒性和线粒体功能.
主要成果:
- 患者活检显示了近道管损伤和纤维化.
- 暴露在有毒物质和 puberulic 酸中的小鼠表现出损伤,管状缩,纤维化和类似 Fanconi 综合征的特征.
- RNA-seq表明 puberulic 酸是致病剂,基因本体学分析显示线粒体通路下调.
- 在hRPTEC和有机体中,puberulic酸诱导了线粒体损伤和细胞死亡,破坏了呼吸代谢.
结论:
- 酸和受污染的红酵母大米补充剂诱导毒性.
- 主要机制涉及线粒体损伤和随后的管状上皮细胞中的细胞死亡.
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