The Pathogenesis of Necroptosis-Dependent Signaling Pathway in Cerebral Ischemic Disease
Necroptosis is the best-described form of regulated necrosis at present, which is widely recognized as a component of caspase-independent cell death mediated by the concerted action of receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3). Mixed-lineage kina...
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| Format: | Article |
| Language: | English |
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Wiley
2018-01-01
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| Series: | Behavioural Neurology |
| Online Access: | http://dx.doi.org/10.1155/2018/6814393 |
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| author | Yang Xu Ji Zhang Lingsong Ma Shoucai Zhao Shizun Li Tingting Huang Zhaohu Chu |
| author_facet | Yang Xu Ji Zhang Lingsong Ma Shoucai Zhao Shizun Li Tingting Huang Zhaohu Chu |
| author_sort | Yang Xu |
| collection | DOAJ |
| description | Necroptosis is the best-described form of regulated necrosis at present, which is widely recognized as a component of caspase-independent cell death mediated by the concerted action of receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3). Mixed-lineage kinase domain-like (MLKL) was phosphorylated by RIPK3 at the threonine 357 and serine 358 residues and then formed tetramers and translocated onto the plasma membrane, which destabilizes plasma membrane integrity leading to cell swelling and membrane rupture. Necroptosis is downstream of the tumor necrosis factor (TNF) receptor family, and also interaction with NOD-like receptor pyrin 3 (NLRP3) induced inflammasome activation. Multiple inhibitors of RIPK1 and MLKL have been developed to block the cascade of signal pathways for procedural necrosis and represent potential leads for drug development. In this review, we highlight recent progress in the study of roles for necroptosis in cerebral ischemic disease and discuss how these modifications delicately control necroptosis. |
| format | Article |
| id | doaj-art-5628f15f35fc4ade95d9c06e4f9a91a6 |
| institution | Kabale University |
| issn | 0953-4180 1875-8584 |
| language | English |
| publishDate | 2018-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Behavioural Neurology |
| spelling | doaj-art-5628f15f35fc4ade95d9c06e4f9a91a62025-02-03T01:06:19ZengWileyBehavioural Neurology0953-41801875-85842018-01-01201810.1155/2018/68143936814393The Pathogenesis of Necroptosis-Dependent Signaling Pathway in Cerebral Ischemic DiseaseYang Xu0Ji Zhang1Lingsong Ma2Shoucai Zhao3Shizun Li4Tingting Huang5Zhaohu Chu6Department of Neurology, First Affiliated Hospital of Wannan Medical College, No. 2, ZheShanXi Road, Wuhu 241001, ChinaDepartment of Neurology, First Affiliated Hospital of Wannan Medical College, No. 2, ZheShanXi Road, Wuhu 241001, ChinaDepartment of Neurology, First Affiliated Hospital of Wannan Medical College, No. 2, ZheShanXi Road, Wuhu 241001, ChinaDepartment of Neurology, First Affiliated Hospital of Wannan Medical College, No. 2, ZheShanXi Road, Wuhu 241001, ChinaDepartment of Neurology, First Affiliated Hospital of Wannan Medical College, No. 2, ZheShanXi Road, Wuhu 241001, ChinaDepartment of Neurology, First Affiliated Hospital of Wannan Medical College, No. 2, ZheShanXi Road, Wuhu 241001, ChinaDepartment of Neurology, First Affiliated Hospital of Wannan Medical College, No. 2, ZheShanXi Road, Wuhu 241001, ChinaNecroptosis is the best-described form of regulated necrosis at present, which is widely recognized as a component of caspase-independent cell death mediated by the concerted action of receptor-interacting protein kinase 1 (RIPK1) and receptor-interacting protein kinase 3 (RIPK3). Mixed-lineage kinase domain-like (MLKL) was phosphorylated by RIPK3 at the threonine 357 and serine 358 residues and then formed tetramers and translocated onto the plasma membrane, which destabilizes plasma membrane integrity leading to cell swelling and membrane rupture. Necroptosis is downstream of the tumor necrosis factor (TNF) receptor family, and also interaction with NOD-like receptor pyrin 3 (NLRP3) induced inflammasome activation. Multiple inhibitors of RIPK1 and MLKL have been developed to block the cascade of signal pathways for procedural necrosis and represent potential leads for drug development. In this review, we highlight recent progress in the study of roles for necroptosis in cerebral ischemic disease and discuss how these modifications delicately control necroptosis.http://dx.doi.org/10.1155/2018/6814393 |
| spellingShingle | Yang Xu Ji Zhang Lingsong Ma Shoucai Zhao Shizun Li Tingting Huang Zhaohu Chu The Pathogenesis of Necroptosis-Dependent Signaling Pathway in Cerebral Ischemic Disease Behavioural Neurology |
| title | The Pathogenesis of Necroptosis-Dependent Signaling Pathway in Cerebral Ischemic Disease |
| title_full | The Pathogenesis of Necroptosis-Dependent Signaling Pathway in Cerebral Ischemic Disease |
| title_fullStr | The Pathogenesis of Necroptosis-Dependent Signaling Pathway in Cerebral Ischemic Disease |
| title_full_unstemmed | The Pathogenesis of Necroptosis-Dependent Signaling Pathway in Cerebral Ischemic Disease |
| title_short | The Pathogenesis of Necroptosis-Dependent Signaling Pathway in Cerebral Ischemic Disease |
| title_sort | pathogenesis of necroptosis dependent signaling pathway in cerebral ischemic disease |
| url | http://dx.doi.org/10.1155/2018/6814393 |
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