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YY1/HIF-1α/mROS正反循环在小鼠早期糖尿病病中加剧了球间细胞的增殖

Ting-Ting Yang¹, Yu-Ting Shao¹, Qian Cheng¹

¹Jiangsu Key Laboratory of New Drug Research and Clinical Pharmacy, Xuzhou Medical University, Xuzhou, 221004, China.

Acta pharmacologica Sinica

|March 4, 2025

概括

阴阳1 (YY1) 通过激活HIF-1α和ROS来驱动糖尿病病中的中细胞增殖. 抑制这种YY1/HIF-1α/mROS通路可能会预防淋巴结核硬化.

科学领域:

腎臟病學 (nephrology) 是一種醫學專業.
分子生物学分子生物学
糖尿病学糖尿病学

背景情况:

糖尿病病 (DKD) 涉及过度的间细胞 (MC) 增殖,导致球膜硬化和功能衰竭.
阴阳1 (YY1) 已被确定为DKD诱导纤维化的调节剂.

研究的目的:

调查YY1在DKD中的球MC增殖中的作用.
阐明YY1对DKD中MC的影响背后的分子机制.

主要方法:

在DKD患者,db/db小鼠和高葡萄糖 (HG) 治疗细胞中评估YY1表达.
利用YY1表达/敲击等离子体来研究其对MC增殖的影响.
研究了YY1对缺氧诱导因子-1α (HIF-1α) 和线粒体活性氧物种 (mROS) 的影响.
研究了对正常和糖尿病小鼠的脏特异性YY1操纵的影响.

主要成果:

在DKD患者,db/db小鼠和HG治疗细胞的球MC中,YY1表达显著增加.
在体外和体内,YY1促进了球MC的扩散.
YY1上调HIF-1α,导致mROS过度产生,形成一个积极的反循环,加剧了MC增殖.
通过抑制HIF-1α/ROS信号传递,脏YY1敲击减轻了早期DKD中的MC增殖.

结论:

阳性YY1/HIF-1α/mROS反循环在早期的DKD中对质MC增殖起着至关重要的作用.
准这种途径为预防DKD中的淋巴结核硬化提供了潜在的治疗策略.

关键词:

在HIF-1α/mROS信号传输中.YY1 YY1 这是一个很大的问题.糖尿病脏病糖尿病脏病介管细胞增殖介管细胞增殖积极的反循环是一个循环.

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