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在MASLD相关的肝细胞癌中,AKR1B1驱动高血糖引起的代谢重编程

N P Syamprasad¹, Siddhi Jain¹, Bishal Rajdev¹

¹Department of Pharmacology & Toxicology, National Institute of Pharmaceutical Education and Research Guwahati, Sila village, Changsari, Assam, 781101, India.

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|January 29, 2024

概括

这项研究揭示了阿尔多减少酶 (AKR1B1) 通过改变肝脏代谢来驱动代谢功能障碍相关的脂肪性肝病 (MASLD) 和肝癌 (HCC) 的进展. 抑制AKR1B1对新的MASLD-HCC治疗和诊断有希望.

科学领域:

肝病学肝病学是一种肝病学.
代谢障碍代谢障碍代谢障碍
在瘤学瘤学.
生物化学生物化学

背景情况:

与代谢功能障碍相关的脂肪性肝病/脂肪性肝炎 (MASLD/MASH) 与肝细胞癌 (HCC) 联系的机制尚不清楚.
研究聚醇途径酶阿尔多减少酶 (AKR1B1) 在代谢变化和HCC进展中的作用至关重要.

研究的目的:

探索AKR1B1在MASLD/MASH中的代谢切换中的功能.
确定AKR1B1在与MASLD相关的HCC的发展和进展中的参与.

主要方法:

在患者组织和血中的AKR1B1表达分析 (MASLD/MASH,HCC,患有糖尿病的HCC).
采用lentiviral传染和药理探针进行体外研究,以评估AKR1B1在代谢切换中的作用.
蛋白质组和代谢组分析,以及临床前小鼠模型 (高果糖饮食,二甲基胺) 来研究AKR1B1在高血糖中介的MASLD-HCC中的功能.

主要成果:

在患有MASLD/MASH,HCC和糖尿病HCC的患者中发现AKR1B1表达升高.
在体外,AKR1B1被证明可以调节华堡效应,线粒体动力学,TCA循环和脂质生成,促进高血糖驱动的MASLD和癌症.
临床前模型证实了AKR1B1在MASLD-HCC中的作用,而epalrestat或NARI-29的抑制降低了细胞代谢.

结论:

病理性AKR1B1驱动肝脏新陈代谢,促进MASLD相关的肝癌发生.
抑制阿尔多缩酶 (AKR1B1) 可以调节糖解路径,可能防止癌前肝细胞的形成.
AKR1B1代表了MASLD和HCC的可用药物标,具有新的化疗剂和血AKR1B1作为预后/诊断标记物的潜力.

关键词:

在HCC中,HCC是HCC,HCC是HCC.这是MASLD/MASH.代谢过程中的代谢.纳里-29号是第一个.华堡效应是什么? 华堡效应甲基二甲酸酸胺的二甲基二甲酸.美国的Epalrestat.高果糖饮食高果糖饮食

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