title: Cell death by necrosis: towards a molecular definition.
abstract: Necrosis has been defined as a type of cell death that lacks the features of apoptosis and autophagy, and is usually considered to be uncontrolled. Recent research suggests, however, that its occurrence and course might be tightly regulated. After signaling- or damage-induced lesions, necrosis can include signs of controlled processes such as mitochondrial dysfunction, enhanced generation of reactive oxygen species, ATP depletion, proteolysis by calpains and cathepsins, and early plasma membrane rupture. In addition, the inhibition of specific proteins involved in regulating apoptosis or autophagy can change the type of cell death to necrosis. Because necrosis is prominent in ischemia, trauma and possibly some forms of neurodegeneration, further biochemical comprehension and molecular definition of this process could have important clinical implications.
authors.affiliation: Centre d'Immunologie de Marseille-Luminy, Université de la Méditerranée, Case 906, 13288 Marseille Cedex 9, France.
authors.forename: Pierre
authors.initials: P
authors.lastname: Golstein
authors.forename: Guido
authors.initials: G
authors.lastname: Kroemer
mesh_terms: D000818:Animals; D017173:Caenorhabditis elegans; D002154:Calpain / Q000502:physiology; D002403:Cathepsins / Q000502:physiology; D016923:Cell Death / Q000502:physiology*; D000081406:Peptidyl-Prolyl Isomerase F; D021983:Cyclophilins / Q000502:physiology; D006801:Humans; D009336:Necrosis / Q000503:physiopathology; D053422:Receptor-Interacting Protein Serine-Threonine Kinases / Q000502:physiology
chemical_list: D000081406:Peptidyl-Prolyl Isomerase F; D053422:Receptor-Interacting Protein Serine-Threonine Kinases; D002403:Cathepsins; D002154:Calpain; D021983:Cyclophilins