An Inflammatory Perspective on Necroptosis
An Inflammatory Perspective on Necroptosis
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DOI：
10.1016/j.molcel.2017.02.024
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发表时间：
2017-03-16
期刊：
影响因子：
16
通讯作者：
Martin, Seamus J.
中科院分区：
文献类型：
--
作者：
Kearney, Conor J.;Martin, Seamus J.
当细胞凋亡所需的半胱天冬酶活性被阻断时，坏死性凋亡（程序性坏死）响应于TNF、Fas或TRAIL以及某些TLR配体而发生。坏死性凋亡通常被认为是一种高度促炎的细胞死亡模式，这是由于细胞内释放促进炎症的“危险信号”。然而，由于大多数促坏死性凋亡刺激本身是高度促炎的-由于它们能够启动许多细胞因子和趋化因子的合成-坏死性凋亡的炎症后果是复杂的。在这里，我们认为，坏死性凋亡可能有抗炎作用，在某些情况下，通过抑制过度的TNF-或TLR诱导的炎症细胞因子的产生。
Necroptosis (programmed necrosis) occurs in response to TNF, Fas, or TRAIL, as well as certain TLR ligands, when caspase activity required for apoptosis is blocked. Necroptosis is typically considered a highly pro-inflammatory mode of cell death, due to release of intracellular "danger signals'' that promote inflammation. However, because most pro-necroptotic stimuli are intrinsically highly pro-inflammatory-due to their ability to initiate the synthesis of numerous cytokines and chemokines-the inflammatory consequences of necroptosis are complex. Here, we suggest that necroptosis might have anti-inflammatory effects in certain settings, through curbing excessive TNF- or TLR-induced inflammatory cytokine production.