IL6 Derived from Macrophages under Intermittent Hypoxia Exacerbates NAFLD by Promoting Ferroptosis via MARCH3‐Led Ubiquitylation of GPX4

间歇性缺氧 非酒精性脂肪肝 阻塞性睡眠呼吸暂停 癌症研究 缺氧(环境) 泛素 医学 内分泌学 内科学 脂肪肝 化学 疾病 基因 生物化学 有机化学 氧气
作者
Weisong Cai,Sa Wu,Xiaoping Ming,Zhen Li,Dingyu Pan,Xiuping Yang,Minlan Yang,Yufeng Yuan,Xiong Chen
出处
期刊:Advanced Science [Wiley]
标识
DOI:10.1002/advs.202402241
摘要

Abstract Obstructive sleep apnea (OSA) is a common sleep disorder characterized by intermittent hypoxia (IH) and is associated with the occurrence and development of nonalcoholic fatty liver disease (NAFLD). However, the specific mechanism by which OSA induces NAFLD remains unclear. Therefore, effective interventions are lacking. This study aims to investigate the role and mechanism of ferroptosis in OSA‐related NAFLD using clinical data analyses, cell‐based molecular experiments, and animal experiments. Indicators of liver function, lipid accumulation, and ferroptosis are also examined. RNA‐seq, qPCR, western blotting, gene intervention, and E3 ligase prediction using UbiBrowser and co‐IP are used to explore the potential underlying mechanisms. The results show that ferroptosis increases in the liver tissues of patients with OSA. Chronic IH promotes NAFLD progression in mice and is alleviated by a ferroptosis inhibitor Fer‐1. The increased secretion of IL6 by macrophages can promote the expression of MARCH3 in hepatocytes under intermittent conditions, and subsequently promote the ubiquitination and degradation of GPX4 to regulate ferroptosis and lipid accumulation in hepatocytes. Hence, targeted inhibition of MARCH3 may alleviate IH‐induced ferroptosis and lipid accumulation in liver tissues and inhibit the progression of NAFLD.
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