期刊
MOLECULAR & CELLULAR ONCOLOGY
卷 2, 期 4, 页码 -出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/23723556.2014.975093
关键词
apoptosis; necroptosis; crosstalk; tumor necrosis factor; Fas; RIPK1; RIPK3; FLIP
类别
资金
- Foundation against Cancer [2012-188]
- European grant (FP6 ApopTrain) [MRTNCT-035624]
- European grant (FP7 EC RTD Integrated Project, Apo-Sys) [FP7-200767]
- European grant (Euregional PACT II)
- Belgian grants (Interuniversity Attraction Poles) [IAP 6/18, IAP 7/32]
- Flemish grants (Research Foundation Flanders) [FWO G.0875.11, FWO G.0973.11 N, FWO G.0A45.12 N, FWO G.0172.12, FWO G.0787.13N, G0C3114N, FWO KAN 31528711]
- Ghent University grants (MRP, GROUP-ID consortium)
- Flanders Institute for Biotechnology (VIB)
- Flemish Government [BOF09/01M00709]
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [DP5OD012198] Funding Source: NIH RePORTER
Our current knowledge of the molecular mechanisms regulating the signaling pathways leading to cell survival, cell death, and inflammation has shed light on the tight mutual interplays between these processes. Moreover, the fact that both apoptosis and necrosis can be molecularly controlled has greatly increased our interest in the roles that these types of cell death play in the control of general processes such as development, homeostasis, and inflammation. In this review, we provide a brief update on the different cell death modalities and describe in more detail the intracellular crosstalk between survival, apoptotic, necroptotic, and inflammatory pathways that are activated downstream of death receptors. An important concept is that the different cell death processes modulate each other by mutual inhibitory mechanisms, serve as alternative back-up death routes in the case of a defect in the first-line cell death response, and are controlled by multiple feedback loops. We conclude by discussing future perspectives and challenges in the field of cell death and inflammation research.
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