高葡萄糖通过BAP1/SLC7A11通路诱导细胞铁
Ren Peiyao1,2, Man Xueli1, Sun Wenbo1
1Department of Nephrology, The First Affiliated Hospital of Zhejiang Chinese Medical University (Zhejiang Provincial Hospital of Traditional Chinese Medicine), Hangzhou, Zhejiang, 310000, PR China.
Heliyon
|January 16, 2025
概括
高葡萄糖通过抑制 podocytes 中的囊吸收来加速糖尿病病中的铁亡. 这通过增加BAP1的表达发生,该表达降低SLC7A11的调节,并促进氧化应激和细胞死亡.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 细胞生物学 细胞生物学
- 生物化学 生物化学
背景情况:
- 铁亡是糖尿病病 (DN) 发展的关键因素.
- 在DN中铁亡的精确调节机制尚未完全理解.
研究的目的:
- 阐明BAP1在高葡萄糖条件下在细胞内的铁亡中的调节作用.
- 调查高葡萄糖对SLC7A11表达的影响及其与糖尿病病中铁亡的关系.
主要方法:
- 在高葡萄糖 (HG) 中培养MPC5细胞以模仿糖尿病状况.
- 测量了铁和氧化应激标志物 (MDA,囊摄取,ROS).
- 使用野生类型和C91A突变细胞研究了BAP1和SLC7A11的相互作用.
主要成果:
- 高葡萄糖加剧了埃拉斯诱导的铁,减少了谷氨和增加了氧化应激.
- HG抑制了SLC7A11的表达,而其过度表达恢复了囊的吸收并减少了氧化应激.
- HG增加了BAP1水平;BAP1沉默调高了SLC7A11和降低了铁亡.
结论:
- 高葡萄糖通过增加BAP1的表达和影响SLC7A11deubiquitination来抑制Podocyte的囊吸收.
- 这导致脂质过氧化物积累和铁,有助于糖尿病病的进展.
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