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肝脏在芯片上的生理氧气梯度区域显示HIF-2α干预肝脏脂毒性

Yushen Wang¹, Xinyu Li², Junlei Han¹

¹School of Mechanical Engineering, Qilu University of Technology (Shandong Academy of Sciences), Jinan 250353, China; Shandong Institute of Mechanical Design and Research, Jinan 250353, China; School of Mechanical Engineering, Shandong Key Laboratory of CNC Machine Tool Functional Components, Qilu University of Technology (Shandong Academy of Sciences), Jinan, Shandong 250353, China.

Acta biomaterialia

|November 27, 2025

概括

研究人员开发了一种模拟氧气梯度的MASLD肝芯片模型. 该模型显示,HIF-2α通过β-catenin和WNT信号传递间接促进MASLD的进展,这表明了新的治疗点.

科学领域:

肝病学和肝脏疾病.
生物工程和芯片器官技术
分子和细胞生理学分子和细胞生理学

背景情况:

代谢功能障碍相关的脂肪性肝病 (MASLD) 的特征是脂质区分,与肝叶功能区分相关.
现有的模型无法复制生理氧度梯度,这对于理解MASLD进展和制定干预措施至关重要.
准确地回顾肝脏微环境,包括氧度梯度,对于研究肝脏病理生理学至关重要.

研究的目的:

为了设计一个MASLD肝脏-zonation-on-a-chip平台,准确地复制体内氧气梯度.
使用开发的芯片,研究氧感应因子,特别是HIF-2α在MASLD进展中的作用.
通过阐明疾病进展的分子机制来确定MASLD的潜在治疗点.

主要方法:

开发使用"环境氧气对流和扩散"策略的肝脏在芯片上的区分.
达到可控制的氧度梯度 (3.7%-8.9%),模仿肝脏微环境.
综合生物传感用于持续,非破坏性监测肝损伤和评估MASLD表型.

主要成果:

工程芯片成功地重现了MASLD的肝叶区分和临床病理特征.
升调HIF-2α并没有直接导致脂质积累,但间接促进了MASLD的进展.
HIF-2α通过WNT信号通路 (AXIN2,DVL1) 增强了β-catenin的转录活性,促进了MASLD的进展.

结论:

芯片上的MASLD肝区划为研究肝脏区划和MASLD病理生理学提供了卓越的模型.
HIF-2α和β-catenin是通过WNT信号通路进行MASLD进展的关键调节剂.
向HIF-2α和β-catenin是一个有希望的治疗策略,可以改善MASLD的结果.

关键词:

氨酸氨基转移酶 (ALT) 传感器的整合针对MASLD的干预机制肝脏的区域化是肝脏的区域化.在芯片上进行肝脏区分.与代谢功能障碍相关的脂肪性肝病 (MASLD)生理学氧气梯度梯度的生理学氧气梯度

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