帕金介导的mitophagy通过TGF-β与肝脏恒星细胞激活有关
Ji Hyun Lee1, Kyu Min Kim1,2, Eun Hee Jung1
1College of Pharmacy, Chosun University, Gwangju 61452, Republic of Korea.
International journal of molecular sciences
|October 14, 2023
概括
通过转化生长因子-β (TGF-β) 诱导的帕金基介导的线粒,通过激活肝星细胞 (HSCs) 来促进肝纤维化. 抑制线粒可能为肝纤维化提供治疗策略.
科学领域:
- 细胞生物学 细胞生物学
- 肝病学 肝病学是一种肝病学.
- 生物化学 生物化学
背景情况:
- 肝星细胞 (HSC) 驱动肝纤维化.
- 帕金是一种E3结合酶,调节了线粒体和线粒体平衡.
- 在肝纤维化中TGF-β,帕金和HSC激活之间的联系尚不清楚.
研究的目的:
- 调查帕金介导的线粒在TGF-β诱导的HSC激活和肝纤维化中的作用.
主要方法:
- 人类和小鼠纤维性肝组织和初级HSCs的免疫染和免疫阻塞.
- 用帕金过度表达和线粒细胞衰变抑制剂刺激LX-2细胞的TGF-β.
- 对基因表达,细胞迁移和线粒体功能进行分析.
主要成果:
- 帕金因在纤维化肝脏和高血压细胞中升级调节,并通过Smad3.3.通过TGF-β诱导.
- TGF-β促进了帕金转移到线粒体,激活了线粒体细胞吸食,但没有改变线粒体的功能.
- 线抑制抑制了TGF-β诱导的益纤维素基因表达和HSC迁移.
结论:
- TGF-β诱导的帕金基媒介性线粒会导致HSC激活和肝纤维化.
- 准帕金介导的线粒化为肝纤维化提供了潜在的治疗途径.
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