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'''Necroptosis''' is a programmed form of necrotic cell death. | '''Necroptosis''' is a programmed form of necrotic cell death. | ||
Necrotic cell death has been considered a form of passive cell death. However, the discovery that [[TNFα]]-mediated [[necrosis]] can be inhibited by a specific inhibitor of [[RIP1 kinase]], necrostatin-1, led to the concept of necroptosis.<ref name="pmid16408008">{{cite journal | author = Degterev A, Huang Z, Boyce M, Li Y, Jagtap P, Mizushima N, Cuny GD, Mitchison TJ, Moskowitz MA, Yuan J | title = Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury | journal = Nat Chem Biol | volume = 1 | issue = 2 | pages = 112–9 |date=May 2005 | pmid = 16408008 | doi=10.1038/nchembio711}}</ref><ref name="pmid18408713">{{cite journal | author = Degterev A, Hitomi J, Germscheid M, Ch'en IL, Korkina O, Teng X, Abbott D, Cuny GD, Yuan C, Wagner G, Hedrick SM, Gerber SA, Lugovskoy A, Yuan J | title = Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury | journal = Nat Chem Biol | volume = 4 | issue = 5 | pages = 313–21 |date=May 2008 | pmid = 18408713 | doi=10.1038/nchembio.83}}</ref><ref name="pmid3438821">{{cite journal |author=Kaczmarek A, Vandenabeele P, Krysko DV |title=Necroptosis: the release of damage-associated molecular patterns and its physiological relevance.|journal=Immunity | Necrotic cell death has been considered a form of passive cell death. However, the discovery that [[TNFα]]-mediated [[necrosis]] can be inhibited by a specific inhibitor of [[RIPK1|RIP1 kinase]], necrostatin-1, led to the concept of necroptosis.<ref name="pmid16408008">{{cite journal | author = Degterev A, Huang Z, Boyce M, Li Y, Jagtap P, Mizushima N, Cuny GD, Mitchison TJ, Moskowitz MA, Yuan J | title = Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury | journal = Nat Chem Biol | volume = 1 | issue = 2 | pages = 112–9 |date=May 2005 | pmid = 16408008 | doi=10.1038/nchembio711}}</ref><ref name="pmid18408713">{{cite journal | author = Degterev A, Hitomi J, Germscheid M, Ch'en IL, Korkina O, Teng X, Abbott D, Cuny GD, Yuan C, Wagner G, Hedrick SM, Gerber SA, Lugovskoy A, Yuan J | title = Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury | journal = Nat Chem Biol | volume = 4 | issue = 5 | pages = 313–21 |date=May 2008 | pmid = 18408713 | doi=10.1038/nchembio.83}}</ref><ref name="pmid3438821">{{cite journal |author=Kaczmarek A, Vandenabeele P, Krysko DV |title=Necroptosis: the release of damage-associated molecular patterns and its physiological relevance.|journal=Immunity|volume= 38 |issue=2 |pages=209–23 |date=February 2013 |pmid=23438821 |doi=10.1016/j.immuni.2013.02.003}}</ref> Necroptosis has now been established as a regulated necrotic cell death pathway controlled by [[RIPK1]] and [[RIPK3]].<ref name="pmid3438821" /><ref name="pmid20045303">{{cite journal | author = Christofferson DE, Yuan J | title = Necroptosis as an alternative form of programmed cell death | journal = Curr. Opin. Cell Biol. | volume = 22 | issue = 2 | pages = 263–8 |date=April 2010 | pmid = 20045303 | pmc = 2854308 | doi = 10.1016/j.ceb.2009.12.003 }}</ref><ref name="pmid22817896">{{cite journal | author = Li J, McQuade T, Siemer AB, Napetschnig J, Moriwaki K, Hsiao YS, Damko E, Moquin D, Walz T, McDermott A, Chan FK, Wu H | title = The RIP1/RIP3 necrosome forms a functional amyloid signaling complex required for programmed necrosis | journal = Cell | volume = 150 | issue = 2 | pages = 339–50 |date=July 2012 | pmid = 22817896 | doi=10.1016/j.cell.2012.06.019}}</ref> Under conditions that are insufficient to trigger [[apoptosis]], [[TNFα]] activates TNFR1 and in turn induces the recruitment of [[RIPK1|RIP1 kinase (RIPK1)]] and other proteins to form complex I. Subsequently, these proteins dissociate from TNFR1 and RIP1 can be found in the [[cytosol]] in complex IIb, which includes [[RIPK1|RIP1]], [[RIPK3|RIP3]], [[caspase 8]] and [[FADD]]. The formation of complex IIb leads to necroptosis.<ref name="pmid20045303"/> | ||
|volume= 38 |issue=2 |pages=209–23 |date=February 2013 |pmid=23438821 |doi=10.1016/j.immuni.2013.02.003}}</ref> | |||
Necroptosis has now been established as a regulated necrotic cell death pathway controlled by [[RIPK1]] and [[RIPK3]].<ref name="pmid3438821" /><ref name="pmid20045303">{{cite journal | author = Christofferson DE, Yuan J | title = Necroptosis as an alternative form of programmed cell death | journal = Curr. Opin. Cell Biol. | volume = 22 | issue = 2 | pages = 263–8 |date=April 2010 | pmid = 20045303 | pmc = 2854308 | doi = 10.1016/j.ceb.2009.12.003 }}</ref><ref name="pmid22817896">{{cite journal | author = Li J, McQuade T, Siemer AB, Napetschnig J, Moriwaki K, Hsiao YS, Damko E, Moquin D, Walz T, McDermott A, Chan FK, Wu H | title = The RIP1/RIP3 necrosome forms a functional amyloid signaling complex required for programmed necrosis | journal = Cell | volume = 150 | issue = 2 | pages = 339–50 |date=July 2012 | pmid = 22817896 | doi=10.1016/j.cell.2012.06.019}}</ref> | |||
Under conditions that are insufficient to trigger [[apoptosis]], [[TNFα]] activates | |||
Necroptosis plays a role in various pathological forms of cell death, including [[Cerebral hypoxia|ischemic brain injury]], [[neurodegenerative disease]]s and [[viral infection]]s.<ref name=Dunai2011>{{cite journal|last=Dunai|first=Z|coauthors=Bauer, PI; Mihalik, R|title=Necroptosis: biochemical, physiological and pathological aspects|journal=Pathol. Oncol. Res.: POR |date=December 2011 |volume=17|issue=4|pages=791–800|pmid=21773880 |doi=10.1007/s12253-011-9433-4}}</ref> | Necroptosis plays a role in various pathological forms of cell death, including [[Cerebral hypoxia|ischemic brain injury]], [[neurodegenerative disease]]s and [[viral infection]]s.<ref name=Dunai2011>{{cite journal|last=Dunai|first=Z|coauthors=Bauer, PI; Mihalik, R|title=Necroptosis: biochemical, physiological and pathological aspects|journal=Pathol. Oncol. Res.: POR |date=December 2011 |volume=17|issue=4|pages=791–800|pmid=21773880 |doi=10.1007/s12253-011-9433-4}}</ref> | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Necroptosis is a programmed form of necrotic cell death.
Necrotic cell death has been considered a form of passive cell death. However, the discovery that TNFα-mediated necrosis can be inhibited by a specific inhibitor of RIP1 kinase, necrostatin-1, led to the concept of necroptosis.[1][2][3] Necroptosis has now been established as a regulated necrotic cell death pathway controlled by RIPK1 and RIPK3.[3][4][5] Under conditions that are insufficient to trigger apoptosis, TNFα activates TNFR1 and in turn induces the recruitment of RIP1 kinase (RIPK1) and other proteins to form complex I. Subsequently, these proteins dissociate from TNFR1 and RIP1 can be found in the cytosol in complex IIb, which includes RIP1, RIP3, caspase 8 and FADD. The formation of complex IIb leads to necroptosis.[4]
Necroptosis plays a role in various pathological forms of cell death, including ischemic brain injury, neurodegenerative diseases and viral infections.[6]
References
- ↑ Degterev A, Huang Z, Boyce M, Li Y, Jagtap P, Mizushima N, Cuny GD, Mitchison TJ, Moskowitz MA, Yuan J (May 2005). "Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury". Nat Chem Biol. 1 (2): 112–9. doi:10.1038/nchembio711. PMID 16408008.
- ↑ Degterev A, Hitomi J, Germscheid M, Ch'en IL, Korkina O, Teng X, Abbott D, Cuny GD, Yuan C, Wagner G, Hedrick SM, Gerber SA, Lugovskoy A, Yuan J (May 2008). "Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury". Nat Chem Biol. 4 (5): 313–21. doi:10.1038/nchembio.83. PMID 18408713.
- ↑ 3.0 3.1 Kaczmarek A, Vandenabeele P, Krysko DV (February 2013). "Necroptosis: the release of damage-associated molecular patterns and its physiological relevance". Immunity. 38 (2): 209–23. doi:10.1016/j.immuni.2013.02.003. PMID 23438821.
- ↑ 4.0 4.1 Christofferson DE, Yuan J (April 2010). "Necroptosis as an alternative form of programmed cell death". Curr. Opin. Cell Biol. 22 (2): 263–8. doi:10.1016/j.ceb.2009.12.003. PMC 2854308. PMID 20045303.
- ↑ Li J, McQuade T, Siemer AB, Napetschnig J, Moriwaki K, Hsiao YS, Damko E, Moquin D, Walz T, McDermott A, Chan FK, Wu H (July 2012). "The RIP1/RIP3 necrosome forms a functional amyloid signaling complex required for programmed necrosis". Cell. 150 (2): 339–50. doi:10.1016/j.cell.2012.06.019. PMID 22817896.
- ↑ Dunai, Z (December 2011). "Necroptosis: biochemical, physiological and pathological aspects". Pathol. Oncol. Res.: POR. 17 (4): 791–800. doi:10.1007/s12253-011-9433-4. PMID 21773880. Unknown parameter
|coauthors=ignored (help)