Ceramide-Induced Apoptosis in Renal Tubular Cells: A Role of Mitochondria and Sphingosine-1-Phoshate

摘要: Ceramide is synthesized upon stimuli, and induces apoptosis in renal tubular cells (RTCs). Sphingosine-1 phosphate (S1P) functions as a survival factor. Thus, the balance of ceramide/S1P determines ceramide-induced apoptosis. Mitochondria play key role for by altered mitochondrial outer membrane permeability (MOMP). enhances oligomerization pro-apoptotic Bcl-2 family proteins, ceramide channel, reduces anti-apoptotic proteins MOM. This process alters MOMP, resulting generation reactive oxygen species (ROS), cytochrome C release into cytosol, caspase activation, regulates through mitogen-activated protein kinases (MAPKs)-dependent -independent pathways. Conversely, MAPKs alter regulating enzymes involving metabolism, affecting Crosstalk between ROS, many signaling pathways Growth factors rescue S1P, including MAPKs. article reviews evidence supporting discusses mitochondria, pathways, crosstalk these regulation RTCs. A balancing S1P strategy preventing growth are also discussed.