nature：线粒体在炎症中的作用

luoziwei

A role for mitochondria in NLRP3 inflammasome activation2 @. l# ?  P- c+ s& V5 _# x
线粒体在NLRP3炎性体活化中的作用3 J( y! Y! L3 b4 R+ f* H% |
Rongbin Zhou,Amir S. Yazdi,Philippe Menu& Jürg Tschopp. y- l9 l' ?% T
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宿主“危险”信号能激发NLRP3炎性体参与验证反应，如感染和代谢异常等信号。有研究表明，来源于非自主细胞器发生的自体吞噬和活性氧（ROS）分别能负反馈和正反馈的方式调节NLRP3炎性体的激活。在这篇文章里，我们证实阻断线粒体吞噬/自我吞噬导致受伤线粒体累积并释放ROS，而且能激活NLRP3炎性体。一般情况下，静态NLRP3炎性体位于内质网，而活化的NLRP3炎性体及其适体ASC就会在核膜缝隙中重新分布，然后它们一起共位于内质网和线粒体。尤其应该注意的是，阻断电控阴离子通道后都能使ROS和活化NLRP3炎性体的活性失调，这就表明，线粒体失调能激活NLRP3炎性体，这也许能够解释线粒体失调引起一系列炎症反应的发生的原因。
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7 ], }+ p3 ^; E0 T& _2 s, M0 uAn inflammatory response initiated by the NLRP3 inflammasome is triggered by a variety of situations of host ‘danger’, including infection and metabolic dysregulation1, 2. Previous studies suggested that NLRP3 inflammasome activity is negatively regulated by autophagy and positively regulated by reactive oxygen species (ROS) derived from an uncharacterized organelle. Here we show that mitophagy/autophagy blockade leads to the accumulation of damaged, ROS-generating mitochondria, and this in turn activates the NLRP3 inflammasome. Resting NLRP3 localizes to endoplasmic reticulum structures, whereas on inflammasome activation both NLRP3 and its adaptor ASC redistribute to the perinuclear space where they co-localize with endoplasmic reticulum and mitochondria organelle clusters. Notably, both ROS generation and inflammasome activation are suppressed when mitochondrial activity is dysregulated by inhibition of the voltage-dependent anion channel. This indicates that NLRP3 inflammasome senses mitochondrial dysfunction and may explain the frequent association of mitochondrial damage with inflammatory diseases.
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dabai22222

A role for mitochondria in NLRP3 inflammasome activation

LiuRoc

谢谢！

hakunamatataa

这篇文章 不是用试剂盒提取的，能告诉我 你在哪看到的么？