IL-33/ST2L信号通过调节内质网膜应激和亡来缓解糖尿病病
Teng Liu1,2, Yu-Qing Jin1, Qi Wang1
1Department of Epidemiology and Statistics, School of Public Health, Hebei Key Laboratory of Environment and Human Health, Hebei Medical University, Shijiazhuang, China.
BMC nephrology
|December 5, 2023
概括
介质素-33 (IL-33) 信号传递通过减少内分泌网膜 (ER) 应激和亡来减少糖尿病病 (DN) 中的损伤. 这表明IL-33是DN的潜在治疗点.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 内分泌学 在内分泌学.
- 免疫学 免疫学 免疫学
背景情况:
- 糖尿病病 (DN) 是糖尿病 (DM) 的严重并发症.
- 细胞内膜网膜 (ER) 应激和亡是DNA的关键病理因素.
- IL-33/ST2轴在DN病原发生中的作用尚未完全理解.
研究的目的:
- 调查IL-33/ST2信号对DN的影响.
- 阐明ER压力和DN中的亡的作用.
- 探索IL-33作为DN的潜在治疗点.
主要方法:
- 在小鼠中诱导的糖尿病脏病是使用链毒素 (STZ) 的.
- 分析了生物化学指数,基因/蛋白质表达 (IL-33/ST2轴,ER压力标志物) 和亡.
- 使用质内皮细胞进行了体外研究.
主要成果:
- 在DN脏中,IL-33水平升高.
- 在实验室中,IL-33治疗减轻了STZ诱导的损伤,并减少了ER压力和亡.
- 可溶性ST2 (sST2) 逆转了IL-33.3的保护作用.
结论:
- 通过抑制ER压力和亡,IL-33/ST2信号减轻DN中的损伤.
- IL-33显示出作为糖尿病病的治疗剂的潜力.
关键词:
细胞灭亡 (apoptosis) 是一种死亡的过程.糖尿病脏病 糖尿病脏病细胞内膜网膜应激压力这里有IL-33和IL-33.ST2 ST2 ST2 ST2 ST2 ST2 ST2 ST2 ST2 ST2 ST2 ST2 ST3 ST4 ST4 ST5 ST6 ST7 ST7 ST7更多相关视频
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