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ERRγ诱导的FGF23通过增强CYP2E1介导的肝氧化应激促进酒精性肝损伤

Yoon Seok Jung¹, Kamalakannan Radhakrishnan¹, Seddik Hammad²

¹Host-derived Antiviral Research Center, School of Biological Sciences and Technology, Chonnam National University, Gwangju 61186, Republic of Korea.

|March 13, 2024

概括

纤维细胞生长因子23 (FGF23) 在酒精性肝病 (ALD) 中被上调. 这项研究揭示了CB1R-ERRγ-FGF23通路通过CYP2E1诱导驱动ALD,这表明FGF23是治疗标.

科学领域:

内分泌学在内分泌学.
肝病学肝病学是一种肝病学.
分子生物学分子生物学

背景情况:

纤维细胞生长因子23 (FGF23) 是一种内分泌激素,主要以酸盐和维生素D代谢而闻名.
最近的发现表明,在病理条件下,FGF23在肝脏中产生,但其在酒精性肝病 (ALD) 中的作用尚不清楚.

研究的目的:

研究肝脏FGF23在ALD病变发生中的作用.
阐明ALD中FGF23调节的基础分子机制.

主要方法:

在ALD患者和健康对照者的肝脏中对FGF23表达的比较分析.
利用肝细胞特异性淘汰赛小鼠对大麻素受体1型 (CB1R),雌激素相关受体玛 (ERRγ) 和FGF23.3进行检测.
用含酒精的饮食和ERRγ逆agonist来评估治疗效果.

主要成果:

在ALD患者的肝脏中,FGF23被上调,在老鼠肝脏中被慢性饮酒诱导.
酒精诱导的肝脏FGF23上调取决于CB1R-ERRγ轴.
通过诱导肝脏CYP2E1,FGF23促进ALD,导致肝细胞亡和氧化应激增加.

结论:

确定了一种新的CB1R-ERRγ-FGF23信号轴,该轴会加剧ALD.
由CYP2E1介导的肝脏FGF23诱导是酒精诱导肝损伤的关键驱动因素.
FGF23代表了治疗酒精性肝病的有前途的治疗标.

关键词:

酒精性肝病是一种肝病.在CYP2E1中.在ERRγ ERRγ 联邦政府财政基金23 氧化应激是一种氧化应激.

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