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巨细胞ATG16L1表达抑制了代谢功能障碍相关的脂肪肝炎的进展,通过促进脂质

Qi Wang^1,2, Qingfa Bu^2,3, Zibo Xu²

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

Clinical and molecular hepatology

|May 10, 2024

概括

与自相关的16样蛋白1 (ATG16L1) 通过增强巨细胞功能来抑制代谢功能障碍相关的脂肪肝炎 (MASH). 促进ATG16L1可能为MASH提供新的治疗策略.

科学领域:

肝病学和免疫学肝病学和免疫学
细胞的新陈代谢
自学研究自学研究

背景情况:

代谢功能障碍相关的脂肪肝炎 (MASH) 是一个日益严重的健康问题,治疗选择有限.
自相关蛋白 16-like 1 (ATG16L1) 在巨介导的炎症和MASH期间代谢中的作用在很大程度上仍未被探索.

研究的目的:

研究MASH进展期间巨细胞中ATG16L1的功能和机制.
确定ATG16L1是否可以成为MASH的治疗点.

主要方法:

来自人类和MASH模型小鼠的肝脏样本的分析 (骨髓特异性Atg16l1缺乏和过度表达).
使用高脂肪/高胆固醇或缺乏氨酸和胆的饮食诱导MASH.
评估巨细胞的自,脂,炎症和代谢途径.

主要成果:

巨细胞特异性ATG16L1缺陷使MASH恶化,并降低了能量消耗.
缺少ATG16L1会损害巨细胞脂质,抑制β-氧化,并通过增加mtDNA吸收促进STING通路的激活.
过度表达ATG16L1减弱了MASH和增加了能量消耗;药物ATG16L1促进阻止了MASH的进展.

结论:

在MASH中,ATG16L1通过维持巨细胞脂质和减少肝炎来发挥保护作用.
向ATG16L1代表了管理MASH的潜在治疗策略.

关键词:

在ATG16L1中使用.脂质性消化 (Lipophagy) 是一种消化方式.巨细胞是一个巨细胞.与代谢功能障碍相关的脂肪肝炎.

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