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衰老加剧肝纤维化通过下调的肝细胞SIRT1诱导的肝脏阴侧内皮细胞功能障碍

Qingqing Dai^1,2, Xin Qing³, Wei Jiang⁴

¹Department of Hepatopancreatobiliary Surgery, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.

Hepatology communications

|December 21, 2023

概括

衰老会通过降低肝细胞Sirtuin 1 (SIRT1),损害肝脏侧侧内皮细胞 (LSECs) 来恶化肝纤维化. 恢复SIRT1可能为肝纤维化提供新的治疗方法.

科学领域:

肝病学肝病学是一种肝病学.
衰老研究研究衰老研究
纤维化机制纤维化机制

背景情况:

衰老加剧慢性肝病和肝纤维化进展.
与衰老,肝病和纤维化有关的机制仍然不完全理解.
调查Sirtuin 1 (SIRT1) 在肝细胞和肝侧内皮细胞 (LSEC) 中的作用至关重要.

研究的目的:

探索衰老和慢性肝病如何影响肝细胞SIRT1和LSEC.
确定这些因素对肝纤维化病原体的贡献.
为了确定与年龄相关的肝纤维化潜在的治疗点.

主要方法:

利用年轻和年老的小鼠模型与四化碳诱导的肝纤维化.
孤立和共同培养的原发性肝星细胞 (HSCs) 和LSECs用于体外研究.
分析了来自人类对照和肝纤维化患者的肝脏组织和血液样本.

主要成果:

在老年小鼠中降低肝细胞SIRT1的调节导致HMGB1乙化和分泌的增加,通过TLR4/AKT/eNOS通路引起LSEC功能障碍,激活HSC并促进纤维化.
肝细胞中的SIRT1过度表达减弱了小鼠的肝损伤和纤维化,使与年龄相关的差异正常化.
在体外,SIRT1过度表达和eNOS激动剂改善了LSEC功能并抑制了HSC激活.
在老年人中观察到肝细胞SIRT1和LSEC功能障碍的减少,在肝纤维化患者中更严重.

结论:

衰老通过降低肝细胞SIRT1的调节加剧肝纤维化,导致LSEC功能障碍.
这种机制突出了预防和治疗肝纤维化的潜在治疗策略.
恢复SIRT1功能是治疗与年龄相关的肝脏疾病的一个有希望的方法.

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