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阻塞性睡眠呼吸暂停综合征加剧通过选择性自介导的Eepd1降解NASH进展

Jie Xiong¹, Ying Xu¹, Ning Wang¹

¹Shanghai Diabetes Institute, Department of Endocrinology and Metabolism, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200233, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|June 26, 2024

概括

阻塞性睡眠呼吸暂停综合征 (OSAS) 通过破坏肝脏DNA,使非酒精性脂肪肝炎 (NASH) 恶化. 准DNA修复酶Eepd1降解为这种情况提供了潜在的治疗策略.

科学领域:

肝病学肝病学是一种肝病学.
睡眠医学睡眠医学
分子生物学分子生物学

背景情况:

阻塞性睡眠呼吸暂停综合征 (OSAS),标志着慢性间歇性缺氧 (CIH),加剧了非酒精性脂肪肝炎 (NASH).
现有的CIH小鼠模型很难准确地反映出由于食物摄入量改变而引起的人类反应.
配对养方法对于研究CIH对NASH发展的影响至关重要.

研究的目的:

研究CIH加剧NASH的机制.
确定DNA修复酶Eepd1在CIH诱导的NASH中的作用.
探索由OSAS加剧的NASH的潜在治疗点.

主要方法:

利用一对被养的小鼠模型来研究CIH对NASH的影响.
进行全基因组关联研究 (GWAS) 以确定相关的基因.
分析了选择性自途径和Eepd1降解.
进行药物查以确定潜在的治疗剂.

主要成果:

CIH暴露导致DNA损伤,肝纤维化和炎症的增加.
GWAS数据将DNA修复酶Eepd1与OSAS联系起来.
CIH诱导了选择性自,降低了Eepd1和恶化了肝细胞DNA损伤.
针对Eepd1肝脏的特定淘汰赛小鼠显示NASH进展恶化.
雷提加二化物抑制了Eepd1降解并减轻了DNA损伤.

结论:

CIH通过Eepd1降解和随后的DNA损伤加剧了NASH.
针对CIH介导的Eepd1降解,为与OSAS相关的NASH提供了潜在的辅助疗法.
Eepd1在防止CIH诱导的肝损伤方面发挥着至关重要的作用.

关键词:

一个CIH的CIH是一个CIH.这是一种DNA修复酶.自性降解的自性降解没有酒精含量的型肝炎.雷蒂加宾二化二

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