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抑制UBQLN1可以通过降低肝细胞中SIKE/p38 MAPK通路的调节来减少MASH的进展

Yifei Chen^1,2, Fuji Yang^1,2, Guojun Zheng³

¹Department of Laboratory Medicine, Wujin Hospital Affiliated with Jiangsu University, Jiangsu University, Changzhou, 213017, China.

Journal of nanobiotechnology

|March 12, 2026

概括

代谢功能障碍相关的脂肪肝炎 (MASH) 涉及UBQLN1促进肝脂积累. 用RBC-EVs@siUBQLN1准UBQLN1为MASH提供了潜在的治疗方法,减少了肥胖症和纤维化.

科学领域:

肝病学肝病学是一种肝病学.
分子生物学分子生物学
代谢疾病代谢疾病

背景情况:

代谢功能障碍相关的脂肪肝炎 (MASH) 是肝硬化和癌症的日益严重的原因.
在MASH中驱动脂质失调的分子机制尚未完全理解.

研究的目的:

研究UBQLN1在MASH中调节肝细胞脂质积累中的作用.
评估UBQLN1向干预措施作为MASH的潜在治疗方法.

主要方法:

临床样本和细胞/动物MASH模型的分析.
利用转录学和LC-MS/MS来研究UBQLN1的机制.
开发并测试红细胞衍生的细胞外囊泡 (RBC-EVs),载有UBQLN1siRNA (RBC-EVs@siUBQLN1).

主要成果:

在MASH患者和小鼠模型中,UBQLN1被上调,与肝脏脂肪相关.
在MASH小鼠中,UBQLN1 knockdown减少了肥胖症,炎症和纤维化.
UBQLN1通过UBQLN1-SIKE-p38 MAPK通路促进脂质的积累.

结论:

UBQLN1-SIKE-p38 MAPK通路在MASH病变发生过程中至关重要.
在体内,RBC-EVs@siUBQLN1有效地减少了肝脏脂肪,改善了MASH的进展.
这项研究确立了针对UBQLN1.1的MASH的新疗法策略.

关键词:

细胞外囊泡中的细胞外囊泡.脂质的积累脂质的积累马什 (MASH) 是一个非常重要的产品.红细胞是血液中的红细胞.UBQLN1 的意思是

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