The cadmium-induced death of mesangial cells results in nephrotoxicity

Liang Yo Yang, Kuan Hsun Wu, Wen Ta Chiu, Sheng Hao Wang, Chwen Ming Shih

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48 引文 斯高帕斯(Scopus)


This study summarizes our most recent findings on the mechanisms underlying the cadmium-induced death of mesangial cells, which leads to nephrotoxicity. Multiple pathways participate in cadmium-induced nephrotoxicity. In the ROS-GSK-3β autophagy pathway, cadmium induces ROS most likely from the mitochondria, and the ROS consequently activate GSK-3β leading to autophagic cell death. In the calcium-ERK autophagy and apoptosis pathway, cadmium stimulates calcium release from the endoplasmic reticulum, which activates ERK leading to predominantly autophagic cell death and a minor level of apoptotic cell death. In the calcium-mitochondria-caspase apoptosis pathway, cadmium-induced elevation of calcium depolarizes the mitochondrial membrane potential and then activates caspase signaling leading to apoptosis. A proposed model for cadmium-induced autophagy and apoptosis leading to nephrotoxicity is summarized in Figure 1.
頁(從 - 到)571-572
出版狀態已發佈 - 5月 16 2009

ASJC Scopus subject areas

  • 細胞生物學
  • 分子生物學


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