Necrosis

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Unlike [[Apoptosis|apoptosis]], programmed cell death, [https://www.sciencedirect.com/topics/neuroscience/necrosis necrosis] occurs when a cell dies prematurely due to trauma, infections or toxins. This causes an inflammatory response, as the cells burst and contents are released<ref>Alberts et al (2008) Molecular Biology of the Cell, 5th Edition, New York: Garland Science, chapter 18</ref>. Necrosis is not reversible and when the large area of the tissue dies due to inefficent blood flow to it this results in [[Gangrene|gangrene]].<ref>MedlinePlus (2013) Necrosis. Available at: http://www.nlm.nih.gov/medlineplus/ency/article/002266.htm (last accessed 28.11.14)</ref>&nbsp;Morphological characteristics of necrosis include increase in cell volume ([[Oncosis|oncosis]]), swelling of organelles, plasma membrane rupture and loss of intracellular contents. For a long time necrosis has been considered as an accidential uncontrolled form of cell death but now there is more evidence that it might be triggered by signal transduction pathways and catabolic mechanisms. It was observed that in the presence of [[Caspase|caspase]] inhibitors, death domain receptors (e.g., [[TNFR1|TNFR1]]) and toll-like receptors (e.g., [[TLR3|TLR3]] and [[TLR4|TLR4]]) evoke necrosis. Knockdown and chemical inhibition with&nbsp;[[Necrostatin-1|necrostatin-1]]&nbsp;revealed that receptors like [[TNFR1|TNFR1]], [[Fas/CD95|Fas/CD95]], [[TRAILR|TRAILR]] and [[TRL3|TRL3]] which mediated cell death were affected by kinase [[RIP1|RIP1]]. However, causative elements of necrosis are still not known<ref>Kroemer G. et al. (2009) Classification of cell death: recommendation of the Nomenclature Committee on Cell Death 2009. Nature 16: 3-11.</ref>.
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Unlike [[Apoptosis|apoptosis]], programmed cell death, necrosis occurs when a cell dies prematurely due to trauma, infections or toxins. This causes an inflammatory response, as the cells burst and contents are released<ref>Alberts et al (2008) Molecular Biology of the Cell, 5th Edition, New York: Garland Science, chapter 18</ref>. Necrosis is not reversible and when the large area of the tissue dies due to inefficent blood flow to it this results in [[Gangrene|gangrene]]<ref>MedlinePlus (2013) Necrosis. Available at: http://www.nlm.nih.gov/medlineplus/ency/article/002266.htm (last accessed 28.11.14)</ref>.&nbsp;Morphological characteristics of necrosis include increase in cell volume ([[Oncosis|oncosis]]), swelling of organelles, plasma membrane rupture and loss of intracellular contents. For a long time necrosis has been considered as an accidential uncontrolled form of cell death but now there is more evidence that it might be triggered by signal transduction pathways and catabolic mechanisms. It was observed that in the presence of [[Caspase|caspase]] inhibitors, death domain receptors (e.g., [[TNFR1|TNFR1]]) and toll-like receptors (e.g., [[TLR3|TLR3]] and [[TLR4|TLR4]]) evoke necrosis. Knockdown and chemical inhibition with&nbsp;[[Necrostatin-1|necrostatin-1]]&nbsp;revealed that receptors like [[TNFR1|TNFR1]], [[Fas/CD95|Fas/CD95]], [[TRAILR|TRAILR]] and [[TRL3|TRL3]] which mediated cell death were affected by kinase [[RIP1|RIP1]]. However, causative elements of necrosis are still not known<ref>Kroemer G. et al. (2009) Classification of cell death: recommendation of the Nomenclature Committee on Cell Death 2009. Nature 16: 3-11.</ref>.  
  
References  
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=== References ===
  
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Latest revision as of 20:45, 6 December 2018

Unlike apoptosis, programmed cell death, necrosis occurs when a cell dies prematurely due to trauma, infections or toxins. This causes an inflammatory response, as the cells burst and contents are released[1]. Necrosis is not reversible and when the large area of the tissue dies due to inefficent blood flow to it this results in gangrene[2]. Morphological characteristics of necrosis include increase in cell volume (oncosis), swelling of organelles, plasma membrane rupture and loss of intracellular contents. For a long time necrosis has been considered as an accidential uncontrolled form of cell death but now there is more evidence that it might be triggered by signal transduction pathways and catabolic mechanisms. It was observed that in the presence of caspase inhibitors, death domain receptors (e.g., TNFR1) and toll-like receptors (e.g., TLR3 and TLR4) evoke necrosis. Knockdown and chemical inhibition with necrostatin-1 revealed that receptors like TNFR1, Fas/CD95, TRAILR and TRL3 which mediated cell death were affected by kinase RIP1. However, causative elements of necrosis are still not known[3].

References

  1. Alberts et al (2008) Molecular Biology of the Cell, 5th Edition, New York: Garland Science, chapter 18
  2. MedlinePlus (2013) Necrosis. Available at: http://www.nlm.nih.gov/medlineplus/ency/article/002266.htm (last accessed 28.11.14)
  3. Kroemer G. et al. (2009) Classification of cell death: recommendation of the Nomenclature Committee on Cell Death 2009. Nature 16: 3-11.

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