期刊
AUTOPHAGY
卷 5, 期 4, 页码 571-572出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/auto.5.4.8311
关键词
cadmium; autophagy; apoptosis; calcium; GSK-3 beta
类别
资金
- Department of Health [DOH-TD-B-111-002]
- Wan Fang Hospital [94TMU-WFH-214]
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-3 beta autophagy pathway, cadmium induces ROS most likely from the mitochondria, and the ROS consequently activate GSK-3 beta 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.
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