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Going up in flames: necrotic cell injury and inflammatory diseases Challa S; Chan FKCell Mol Life Sci 2010[Oct]; 67 (19): 3241-53Recent evidence indicates that cell death can be induced through multiple mechanisms. Strikingly, the same death signal can often induce apoptotic as well as non-apoptotic cell death. For instance, inhibition of caspases often converts an apoptotic stimulus to one that causes necrosis. Because a dedicated molecular circuitry distinct from that controlling apoptosis is required for necrotic cell injury, terms such as "programmed necrosis" or "necroptosis" have been used to distinguish stimulus-dependent necrosis from those induced by non-specific traumas (e.g., heat shock) or secondary necrosis induced as a consequence of apoptosis. In several experimental models, programmed necrosis/necroptosis has been shown to be a crucial control point for pathogen- or injury-induced inflammation. In this review, we will discuss the molecular mechanisms that regulate programmed necrosis/necroptosis and its biological significance in pathogen infections, drug-induced cell injury, and trauma-induced tissue damage.|*Necrosis[MESH]|Animals[MESH]|Apoptosis/physiology[MESH]|Caspases/metabolism[MESH]|Cell Death[MESH]|Cells/metabolism[MESH]|Humans[MESH]|Inflammation[MESH]|Signal Transduction[MESH] |
