Fujiki Kota
Department of Hygiene and Public Health, Tokyo Women's Medical University.
Nihon Eiseigaku Zasshi. 2020;75(0). doi: 10.1265/jjh.20007.
Renal tubular cell death is caused by various extracellular stresses including toxic amounts of cadmium, an occupational and environmental pollutant metal, and is responsible for renal dysfunction. While cadmium exposure disrupts many intracellular signaling pathways, the molecular mechanism underlying cadmium-induced renal tubular cell death has not yet been fully elucidated. We have recently identified two important intracellular signaling pathways that promote cadmium-induced renal tubular cell death: the Notch1 signaling and activin receptor-like kinase (ALK) 4/5 signaling (also known as the activin-transforming growth factor β receptor pathways). In this review paper, we introduce our previous experimental findings, focusing on Notch1 and ALK4/5 signaling pathways, which may uncover the molecular mechanisms involved in cadmium-induced renal tubular cell death.
肾小管细胞死亡是由多种细胞外应激因素引起的，包括有毒剂量的镉（一种职业和环境污染物金属），并且是肾功能障碍的原因。虽然镉暴露会破坏许多细胞内信号通路，但镉诱导肾小管细胞死亡的分子机制尚未完全阐明。我们最近发现了两条促进镉诱导肾小管细胞死亡的重要细胞内信号通路：Notch1信号通路和激活素受体样激酶（ALK）4/5信号通路（也称为激活素 - 转化生长因子β受体通路）。在这篇综述文章中，我们介绍我们之前的实验结果，重点关注Notch1和ALK4/5信号通路，这可能揭示镉诱导肾小管细胞死亡所涉及的分子机制。
