Abstract:
: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-3beta autophagy pathway, cadmium induces ROS most likely from the mitochondria, and the ROS consequently activate GSK-3beta 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.
journal_name
Autophagyjournal_title
Autophagyauthors
Yang LY,Wu KH,Chiu WT,Wang SH,Shih CMdoi
10.4161/auto.5.4.8311subject
Has Abstractpub_date
2009-05-01 00:00:00pages
571-2issue
4eissn
1554-8627issn
1554-8635pii
8311journal_volume
5pub_type
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