The Role of Necroptosis in Cardiovascular Disease
A newly discovered mechanism of cell death, programmed necrosis (necroptosis), combines features of both necrosis and apoptosis. Necroptosis is tightly modulated by a series of characteristic signaling pathways. Activating necroptosis by ligands of death receptors requires the kinase activity of rec...
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doaj-120f449f9d2e49fbb5db3011e882ddc42020-11-24T21:41:30ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122018-07-01910.3389/fphar.2018.00721329814The Role of Necroptosis in Cardiovascular DiseaseShi Zhe-Wei0Ge Li-Sha1Li Yue-Chun2Department of Cardiology, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, ChinaDepartment of Pediatrics, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, ChinaDepartment of Cardiology, The Second Affiliated Hospital and Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou, ChinaA newly discovered mechanism of cell death, programmed necrosis (necroptosis), combines features of both necrosis and apoptosis. Necroptosis is tightly modulated by a series of characteristic signaling pathways. Activating necroptosis by ligands of death receptors requires the kinase activity of receptor-interacting protein 1 (RIP1), which mediates the activation of receptor-interacting protein 3 (RIP3) and mixed lineage kinase domain-like (MLKL) two critical downstream mediators of necroptosis. Recently, different cytokines have been found participating in this mechanism of cell death. Necroptosis has been proposed as an important component to the pathophysiology of heart disease such as vascular atherosclerosis, ischemia-reperfusion injury, myocardial infarction and cardiac remodeling. Targeting necroptosis signaling pathways may provide therapeutic benefit in the treatment of cardiovascular diseases.https://www.frontiersin.org/article/10.3389/fphar.2018.00721/fullnecroptosisvascular atherosclerosisischemia-reperfusion injurycardiac remodelingRIP1/RIP3/MLKL signaling pathway |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Shi Zhe-Wei Ge Li-Sha Li Yue-Chun |
spellingShingle |
Shi Zhe-Wei Ge Li-Sha Li Yue-Chun The Role of Necroptosis in Cardiovascular Disease Frontiers in Pharmacology necroptosis vascular atherosclerosis ischemia-reperfusion injury cardiac remodeling RIP1/RIP3/MLKL signaling pathway |
author_facet |
Shi Zhe-Wei Ge Li-Sha Li Yue-Chun |
author_sort |
Shi Zhe-Wei |
title |
The Role of Necroptosis in Cardiovascular Disease |
title_short |
The Role of Necroptosis in Cardiovascular Disease |
title_full |
The Role of Necroptosis in Cardiovascular Disease |
title_fullStr |
The Role of Necroptosis in Cardiovascular Disease |
title_full_unstemmed |
The Role of Necroptosis in Cardiovascular Disease |
title_sort |
role of necroptosis in cardiovascular disease |
publisher |
Frontiers Media S.A. |
series |
Frontiers in Pharmacology |
issn |
1663-9812 |
publishDate |
2018-07-01 |
description |
A newly discovered mechanism of cell death, programmed necrosis (necroptosis), combines features of both necrosis and apoptosis. Necroptosis is tightly modulated by a series of characteristic signaling pathways. Activating necroptosis by ligands of death receptors requires the kinase activity of receptor-interacting protein 1 (RIP1), which mediates the activation of receptor-interacting protein 3 (RIP3) and mixed lineage kinase domain-like (MLKL) two critical downstream mediators of necroptosis. Recently, different cytokines have been found participating in this mechanism of cell death. Necroptosis has been proposed as an important component to the pathophysiology of heart disease such as vascular atherosclerosis, ischemia-reperfusion injury, myocardial infarction and cardiac remodeling. Targeting necroptosis signaling pathways may provide therapeutic benefit in the treatment of cardiovascular diseases. |
topic |
necroptosis vascular atherosclerosis ischemia-reperfusion injury cardiac remodeling RIP1/RIP3/MLKL signaling pathway |
url |
https://www.frontiersin.org/article/10.3389/fphar.2018.00721/full |
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