Necrosis-dependent and independent signaling of the RIP kinases in inflammation.
Necrosis-dependent and independent signaling of the RIP kinases in inflammation.
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DOI：
10.1016/j.cytogfr.2013.12.013
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发表时间：
2014-04
影响因子：
13
通讯作者：
Chan, Francis K. M.
中科院分区：
文献类型：
--
作者：
Moriwaki, Kenta;Chan, Francis K. M.
现在广泛接受的是，某些形式的坏死是由各种细胞表面和细胞内受体触发的专用信号通路控制的。这种受调节的坏死形式由受体相互作用蛋白激酶1（RIP 1/RIPK 1）和/或RIP 3/RIPK 3的激酶活性介导。许多使用RIP 1激酶抑制剂Necrostatin-1（Nec-1）及其衍生物或RIP 3缺陷小鼠的研究表明，RIP 1和RIP 3参与各种感染性和无菌性炎症疾病。因此，这些特定的表型被解释为依赖于坏死。然而，新的证据表明，RIP 1激酶活性和RIP 3也可以控制细胞凋亡和炎症细胞因子的产生，而不依赖于坏死。因此，我们可能需要重新解释基于体内模型中RIP 1或RIP 3功能丧失得出的结论。我们建议对RIP 1和RIP 3在不同炎症反应中的研究需要考虑RIP激酶的细胞死亡依赖性和独立机制。
It is now widely accepted that some forms of necrosis are controlled by a dedicated signaling pathway triggered by various cell surface and intracellular receptors. This regulated form of necrosis is mediated by the kinase activity of receptor-interacting protein kinase 1 (RIP1/RIPK1) and/or RIP3/RIPK3. A number of studies using the RIP1 kinase inhibitor Necrostatin-1 (Nec-1) and its derivatives, or RIP3-deficient mice demonstrated that RIP1 and RIP3 are involved in various infectious and sterile inflammatory diseases. As a consequence, these specific phenotypes were construed to depend on necrosis. However, emerging evidence indicates that the RIP1 kinase activity and RIP3 can also control apoptosis and inflammatory cytokine production independent of necrosis. Therefore, we may need to re-interpret conclusions drawn based on loss of RIP1 or RIP3 functions in in vivo models. We propose that studies of RIP1 and RIP3 in different inflammatory responses need to consider cell death-dependent and independent mechanisms of the RIP kinases.
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