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河马-YAP1/HIF-1α通路调解了引起的纤维化

Wei Di¹, Yan Li², Lei Zhang¹

¹Key Laboratory of Environmental Stress and Chronic Disease Control and Prevention, Ministry of Education, China Medical University, Shenyang, Liaoning, 110122, China; The Key Laboratory of Liaoning Province on Toxic and Biological Effects of Arsenicy, Shenyang, Liaoning, 110122, China; Department of Environmental Health, School of Public Health, China Medical University, Shenyang, Liaoning, 110122, China.

Environmental research

|June 6, 2024

概括

暴露通过抑制Hippo通路促进纤维化,导致YAP1.1.增加. 这种YAP1与HIF-1α相互作用,驱动纤维化,并可能提供治疗点.

科学领域:

毒理学毒理学毒理学
腎臟病學 (nephrology) 是一種醫學專業.
分子生物学分子生物学

背景情况:

流行病学研究将暴露与慢性病 (CKD) 风险联系起来.
引起的纤维化背后的确切机制,特别是缺氧的作用,仍然不清楚.

研究的目的:

阐明诱导纤维化的分子机制.
研究Hippo信号通路和缺氧诱导因子1α (HIF-1α) 在中介损伤中的作用.

主要方法:

小鼠和人类细胞 (HK-2) 暴露于不同度的酸 (NaAsO2).
分析了HIF-1α,LATS1和YAP1的蛋白质表达水平.
研究了YAP1和HIF-1α之间的相互作用.

主要成果:

暴露增加了和HK-2细胞中的HIF-1α表达.
通过降低LATS1和增加脱酸YAP1.1,抑制了Hippo通路.
观察到YAP1的核转位,YAP1与HIF-1α形成复合体,使其稳定.

结论:

引起的纤维化包括抑制Hippo通路和随后的YAP1激活.
YAP1通过稳定HIF-1α. 在介导纤维化中发挥关键作用.
YAP1代表了引起的病脏疾病的潜在治疗标.

关键词:

亚是一种.在CKD中,它是最好的.纤维化纤维化纤维化这就是HIF-1α.一个YAP1一个YAP1

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