Title |
The Role of Necroptosis in Cardiovascular Disease
|
---|---|
Published in |
Frontiers in Pharmacology, July 2018
|
DOI | 10.3389/fphar.2018.00721 |
Pubmed ID | |
Authors |
Shi Zhe-Wei, Ge Li-Sha, Li Yue-Chun |
Abstract |
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. |
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Geographical breakdown
Country | Count | As % |
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Canada | 1 | 50% |
Unknown | 1 | 50% |
Demographic breakdown
Type | Count | As % |
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Scientists | 1 | 50% |
Members of the public | 1 | 50% |
Mendeley readers
Geographical breakdown
Country | Count | As % |
---|---|---|
Unknown | 86 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
---|---|---|
Student > Bachelor | 15 | 17% |
Student > Ph. D. Student | 14 | 16% |
Student > Master | 6 | 7% |
Researcher | 5 | 6% |
Student > Doctoral Student | 4 | 5% |
Other | 13 | 15% |
Unknown | 29 | 34% |
Readers by discipline | Count | As % |
---|---|---|
Biochemistry, Genetics and Molecular Biology | 25 | 29% |
Medicine and Dentistry | 10 | 12% |
Pharmacology, Toxicology and Pharmaceutical Science | 9 | 10% |
Agricultural and Biological Sciences | 6 | 7% |
Immunology and Microbiology | 3 | 3% |
Other | 4 | 5% |
Unknown | 29 | 34% |