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• W2133669258 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. 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. apoptosis-inducing factor, a flavoprotein normally located in the mitochondrial intermembrane space that can translocate to the nucleus on induction of cell death. Mitochondrial AIF participates in local redox homeostasis, whereas nuclear AIF can contribute to chromatin condensation and degradation. a survival kinase (also called protein kinase B or PKB) that, when activated, indirectly enhances glucose metabolism and suppresses autophagy through the mTOR kinase. a family of evolutionarily conserved genes, whose products are essential for different steps of the autophagic process. One of these genes encodes Atg6, which is also known as Beclin-1. the prototypic anti-apoptotic protein of the Bcl-2 family. The Bcl-2 protein is inserted in the outer mitochondrial membrane and protects mitochondria against MMP. the pro-apoptotic multidomain proteins of the Bcl-2 family. Bax and/or Bak are often required for the apoptosis-specific outer MMP. Whereas Bak is pre-inserted in the outer mitochondrial membrane, Bax has to translocate from the cytosol to mitochondria to mediate MMP. lysomal membrane permeabilization, a process leading to leakage of catabolic enzymes from the lysosomal lumen, is induced by ROS, sphingolipids and lysosomotropic agents. mitochondrial membrane permeabilization, a process affecting both mitochondrial membranes to a variable extent, leading to disruption of mitochondrial structure and function. Outer MMP leads to leakage of intermembrane proteins from mitochondria. Inner MMP is linked to bioenergetic failure caused by loss of the inner mitochondrial transmembrane potential. reactive oxygen species, a side product of normal oxidative phosphorylation that need to be scavenged by the anti-oxidant system of the cell. ROS can be overproduced during deleterious and pathological processes. a plasma membrane Na+/Ca2+ exchanger required for maintaining physiological low levels of Ca2+ in neurons. a process leading to the permeabilizaton of the inner mitochondrial membrane to solutes to up to 1500 Da, causing dissipation of the inner mitochondrial transmembrane potential, colloid osmotic swelling of the mitochondrial matrix and physical dysruption of the outer mitochondrial membrane. a specific kinase that is recruited to the death-inducing signaling complex after occupation of the TNF-R1, and that on activation can mediate various effects including the induction of necrosis. tumor-necrosis factor-α, an inflammatory cytokine that can cause cell death by acting on a specific cell-surface receptor." @default.
• W2133669258 created "2016-06-24" @default.
• W2133669258 creator A5075296559 @default.
• W2133669258 creator A5079533029 @default.
• W2133669258 date "2007-01-01" @default.
• W2133669258 modified "2023-10-14" @default.
• W2133669258 title "Cell death by necrosis: towards a molecular definition" @default.
• W2133669258 cites W1506034405 @default.
• W2133669258 cites W1523845694 @default.
• W2133669258 cites W1600186066 @default.
• W2133669258 cites W1782545213 @default.
• W2133669258 cites W1964390988 @default.
• W2133669258 cites W1964420304 @default.
• W2133669258 cites W1964483580 @default.
• W2133669258 cites W1966081420 @default.
• W2133669258 cites W1970577953 @default.
• W2133669258 cites W1975087901 @default.
• W2133669258 cites W1976282457 @default.
• W2133669258 cites W1986978728 @default.
• W2133669258 cites W1987695408 @default.
• W2133669258 cites W2002099577 @default.
• W2133669258 cites W2002237070 @default.
• W2133669258 cites W2009272717 @default.
• W2133669258 cites W2012985988 @default.
• W2133669258 cites W2017855147 @default.
• W2133669258 cites W2020548763 @default.
• W2133669258 cites W2021678802 @default.
• W2133669258 cites W2023073081 @default.
• W2133669258 cites W2024795929 @default.
• W2133669258 cites W2032444047 @default.
• W2133669258 cites W2036181141 @default.
• W2133669258 cites W2036505818 @default.
• W2133669258 cites W2038266165 @default.
• W2133669258 cites W2038440451 @default.
• W2133669258 cites W2040546382 @default.
• W2133669258 cites W2045810049 @default.
• W2133669258 cites W2055388969 @default.
• W2133669258 cites W2055793916 @default.
• W2133669258 cites W2063099262 @default.
• W2133669258 cites W2067985632 @default.
• W2133669258 cites W2068048197 @default.
• W2133669258 cites W2072756792 @default.
• W2133669258 cites W2074800090 @default.
• W2133669258 cites W2074982435 @default.
• W2133669258 cites W2087140031 @default.
• W2133669258 cites W2087261949 @default.
• W2133669258 cites W2088629175 @default.
• W2133669258 cites W2104205504 @default.
• W2133669258 cites W2106917466 @default.
• W2133669258 cites W2107931679 @default.
• W2133669258 cites W2110476295 @default.
• W2133669258 cites W2110796758 @default.
• W2133669258 cites W2111951684 @default.
• W2133669258 cites W2115772647 @default.
• W2133669258 cites W2116176075 @default.
• W2133669258 cites W2119828989 @default.
• W2133669258 cites W2120531949 @default.
• W2133669258 cites W2123455365 @default.
• W2133669258 cites W2129194265 @default.
• W2133669258 cites W2129438961 @default.
• W2133669258 cites W2130407823 @default.
• W2133669258 cites W2133000461 @default.
• W2133669258 cites W2133169035 @default.
• W2133669258 cites W2135325091 @default.
• W2133669258 cites W2142237620 @default.
• W2133669258 cites W2149388384 @default.
• W2133669258 cites W2153885285 @default.
• W2133669258 cites W2154184264 @default.
• W2133669258 cites W2156682516 @default.
• W2133669258 cites W2159882838 @default.
• W2133669258 cites W2263706743 @default.
• W2133669258 cites W2323474745 @default.
• W2133669258 cites W2332955794 @default.
• W2133669258 cites W4254283855 @default.
• W2133669258 doi "https://doi.org/10.1016/j.tibs.2006.11.001" @default.
• W2133669258 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17141506" @default.
• W2133669258 hasPublicationYear "2007" @default.
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