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首页> 外文期刊>Journal of Molecular Biology >The NLRP3 Inflammasome Renders Cell Death Pro-inflammatory
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The NLRP3 Inflammasome Renders Cell Death Pro-inflammatory

机译：NLRP3炎性炎性促使细胞死亡促炎

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摘要

Abstract NLRP3 is the most studied inflammasome sensor due to its crucial involvement in sterile and infection-triggered inflammation. Although its molecular mode of activation remains to be defined, it is well established that low intracellular potassium concentrations result in its activation. This functionality allows the classical NLRP3 pathway to serve as a highly sensitive, but non-specific surveillance mechanism responding to any type of perturbation that breaches plasma membrane integrity and the associated potassium gradient across the membrane. Here, we review our current knowledge on potassium efflux-dependent NLRP3 activation, with a special focus on how major cell death programs are rendered pro-inflammatory by secondary NLRP3 activation. Apart from the “alternative inflammasome” as the major exception to the rule, this connection explains the fundamental importance of NLRP3 in cell death-associated inflammation and firmly establishes NLRP3 as a principal surveillance mechanism of cellular integrity. Graphical abstract Display Omitted Highlights ? NLRP3 is activated by low intracellular potassium levels. ? This pathway serves as a surveillance mechanism of plasma membrane integrity. ? Due to this functionality, major forms of programmed cell death result in secondary NLRP3 activation.
机译：摘要NLRP3是最受欢迎的炎性炎症传感器，因为其关键涉及无菌和感染触发的炎症。尽管其分子的活化模式仍有待定义，但很好地确定了低细胞内钾浓度导致其活化。该功能允许经典的NLRP3途径用作高度敏感，但非特异性的监测机制响应任何类型的扰动，这些机制违反了膜穿过膜的血浆膜完整性和相关的钾梯度。在这里，我们审查了目前关于磷酸钾依赖性NLRP3激活的知识，特别关注主要细胞死亡计划如何通过次级NLRP3激活使得主要炎症。除了“替代炎症”作为规则的主要例外之外，该联系解释了NLRP3在细胞死亡相关炎症中的基本重要性，并将NLRP3牢固地建立为细胞完整性的主要监测机制。图形抽象显示省略了亮点？ NLRP3由低细胞内钾水平激活。还是该途径用作质膜完整性的监测机制。还是由于这种功能，主要形式的编程细胞死亡导致次级NLRP3激活。

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