慢性饮酒会通过整体蛋白β1/JNK信号传递加剧急性损伤
Zhanji Zhan1, Jiongcheng Chen1, Hong Zhou1
1State Key Laboratory of Organ Failure Research, Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou, China; National Clinical Research Center of Kidney Disease, Guangdong Provincial Institute of Nephrology, Guangzhou, China.
Redox biology
|October 8, 2024
概括
在雌性小鼠中,酒精消费加剧了急性损伤 (AKI),因为它激活了乙甲/整体素β1/JNK信号传递. 这一途径增加了功能障碍和细胞亡,突显了与酒精有关的损伤的性别特异性脆弱性.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學.
- 毒理学 毒理学 毒理学
- 分子生物学分子生物学
背景情况:
- 滥用酒精是一种全球性健康问题,与许多疾病有关.
- 酒精消费对急性损伤 (AKI) 的影响尚不清楚.
- 酒精对损伤的性别特异性影响还不清楚.
研究的目的:
- 为了研究慢性和暴饮暴饮酒对急性损伤 (AKI) 在缺血-再输液损伤 (IRI) 后的影响.
- 阐明潜在的分子机制,特别是整合素β1和JNK信号传递的作用,以及乙甲的参与.
- 为了确定酒精诱导的AKI中潜在的性别差异.
主要方法:
- 在雌性和雄性小鼠中,慢性和暴饮暴食的乙醇食,其次是IRI.
- 评估功能障碍,组织病理学和管状细胞亡.
- RNA测序,西式涂抹和体外细胞培养实验,以分析整合蛋白β1,JNK酸化和乙甲的影响.
主要成果:
- 乙醇食加剧了AKI,其特点是功能障碍增加,严重的组织病理学和增加的管状细胞亡,特别是在雌性小鼠中.
- 确定了整合素β1/JNK信号通路的激活是加剧乙醇养雌性小鼠AKI的关键机制.
- 在乙醇养的雌性小鼠中升的乙甲基被发现直接激活整合蛋白β1/JNK信号传递,并在体外诱导管状细胞亡.
结论:
- 饮酒增加了雌性小鼠对AKI的敏感性,与雄性小鼠相比.
- 乙甲/整蛋白β1/JNK信号级联是女性酒精诱导损伤的关键调解者.
- 这些发现揭示了酒精相关脏损伤的新型性别特异性机制,表明了潜在的治疗点.
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