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肝细胞铁代谢的差异是肝细胞铁灭性变态的基础

Hui Tao, Hamid Y Dar, Cheng Tian

bioRxiv : the preprint server for biology

|July 10, 2023

概括

男性肝细胞比女性更容易受到铁亡 (铁媒介细胞死亡) 的影响,这是由于铁处理的差异. 这项研究揭示了导致肝脏疾病性变态的机制.

科学领域:

肝病学肝病学是一种肝病学.
细胞死亡机制细胞死亡机制
铁的新陈代谢铁的新陈代谢

背景情况:

与女性相比,男性的肝损伤和肝脏疾病的发病率和严重程度更高,其潜在机制尚不清楚.
铁,一种由铁介导的脂质过氧化驱动的调节性细胞死亡形式,与肝脏疾病的发病有关.

研究的目的:

为了研究肝细胞铁死中的潜在性别差异.
通过ferroptosis阐明通过肝脏疾病导致性变态的机制.

主要方法:

对雄性和雌性肝细胞对铁灭诱导剂 (铁,RSL3,iFSP1) 的脆弱性进行比较.
分析线粒体铁 (Fe 2+) 和活性氧物种 (ROS) 水平.
评估铁相关蛋白表达 (TfR1,Mfrn1,FTH1) 和操纵通过基因沉默/敲击在HepG2细胞.
对卵巢切除术 (OVX) 对肝细胞铁和相关分子变化的影响的评估.

主要成果:

男性肝细胞表现出明显更高的脆弱性比女性肝细胞对铁亡.
与女性相比,男性肝细胞表现出线粒体Fe 2+和线粒体ROS (mtROS) 的增加.
女性肝细胞显示铁进口体 (TfR1,Mfrn1) 的表达较低,铁储存蛋白 (FTH1) 的表达较高.
卵巢切除 (OVX) 增强了肝细胞对铁亡的抵抗力,与TfR1降低,FTH1增加和通过ERK依赖途径提高FSP1表达相关.

结论:

雄性和雌性之间的肝细胞铁处理差异有助于ferroptosis中的性二态.
由OVX诱导的升高的FSP1通过减少线粒体铁和mtROS来抑制铁,呈现出一种新的抑制机制.

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