Necrosis is the premature death of cells in living tissue and can be caused by external factors to the cell or tissue, such as infection, toxins, cancer, infarction, poisons, ROS (Reactive Oxygen Species), inflammation or trauma. Historically, cell death has been subdivided into regulated (apoptosis, aka programmed cell death) and unregulated (necrosis) forms. While apoptosis has always been recognized to be a pathway of highly coordinated signaling events which is a naturally occurring cause of cellular death and can often provide beneficial effects to the organism.

Necrosis is morphologically characterized by a gain in cell volume (oncosis), swelling of organelles, plasma membrane rupture and subsequent loss of intracellular contents. Necrosis or necrotic cell death is almost always detrimental and can be fatal. Currently, necrotic pathways are poorly defined and are still largely identified in negative terms by the absence of apoptotic or autophagic markers. Biochemically it is characterized by loss of regulation in ion homeostasis, random digestion of DNA & ultimately postlytic of DNA fragmentation. Physiologically, necrosis affects groups of contiguous cells, phagocytosis by macrophages and significant inflammatory immune response.



Newly research is determining that necrosis is not just a series of unregulated, uncontrollable processes but is in fact a series of 'programmed necrosis' named  necroptosis. Historically, Necrosis has been considered an accidental cell death and not set to determined pathways or cellular regulation. Necrotic cell death is defined by an increase in cell volume, swelling of organelles, plasma membrane rupture and eventual leakage of intracellular components. Now it is becoming increasingly realized, Neurotic cell death may be executed through defined mechanisms or pathways aptly termed "Necroptosis" (Degterev et al 2005). In fact, it may be executed via stimulation of tumor necrosis factor alpha (TNFα), FasL and TRAIL. These are the same ligands that activate apoptosis. 

Thus, cell death induced by the activation of the death receptor may be accomplished through alternative death pathways ornecroptosis. Receptor interacting protein (RIP) kinases constitute a family of seven members, all of which contain a kinase domain (KD). They are crucial regulators of cell survival and death. Specifically, RIP1 kinase activation is required as an upstream regulator of necroptotic death pathway. Additionally, after TNFα stimulation identified Cylindromatosis (CYLD), a tumor suppressor, as an important regulator for mediating both Apoptosis & Necroptosis. It appears ubiquitination/deubiquination may be involved in the signal transduction of both Apoptosis & Necroptosis. 


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