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NATURE：帕金森相关蛋白可缓解炎症

2018-08-25 海北 MedSci原创

帕金森炎症
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虽然帕金森病患者的血清中含有大量促炎细胞因子，包括IL-6，TNF，IL-1β和IFNγ，但炎症是神经元丢失的原因或者结果仍然是未知的。

虽然帕金森病患者的血清中含有大量促炎细胞因子，包括IL-6，TNF，IL-1β和IFNγ，但炎症是神经元丢失的原因或者结果仍然是未知的。
已有的研究显示，parkin（一种E3泛素连接酶）和PINK1（一种泛素激酶）的突变能够导致早发性帕金森病。 PINK1和parkin都在相同的生化途径中起作用，并通过线粒体自噬（一种选择性形式的自噬）帮助细胞去除受损的线粒体。然而，线粒体自噬的体内作用尚不清楚，部分原因是缺乏PINK1或parkin的小鼠没有实质性的帕金森病相关表型。
线粒体应激可以导致损伤相关分子模式（DAMPs）的释放，激活先天免疫，这表明线粒体自噬可以减轻炎症。
最近，来自美国国立卫生研究院的研究人员发现，锻炼后的Prkn - / - 和Pink1 - / - 小鼠以及Prkn - / - ; mutator小鼠表现出强烈炎症表型。Prkn - / - ; mutator小鼠会在线粒体DNA（mtDNA）中积累突变。
由力竭运动或mtDNA突变引起的炎症可以通过STING的同时丧失而完全挽救，STING是I型干扰素对胞质DNA的反应的关键调节剂。
在老年Prkn - / - ;mutator小鼠中观察到的来自黑质致密部的多巴胺能神经元的丧失和运动缺陷也可以通过STING的丧失而被挽救，表明炎症促进了这种表型。具有单和双等位基因PRKN突变的人中也发现了升高的细胞因子。
这些结果支持PINK1-和parkin介导的线粒体自噬在抑制先天免疫中的作用。

原始出处：
Sliter DA et al. Parkin and PINK1 mitigate STING-induced inflammation. NATURE 2018, DOI: 10.1038/s41586-018-0448-9

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    2018-10-10 liye789132251

    #Nat#

    0

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    2018-08-27 lofter

    学习了感谢分享

    0

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    2018-08-26 liumin1987

    嗯嗯，学习了。

    0

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    2018-08-26 chinadoctorliu_19344479

    学习了，谢谢

    0

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    2018-08-25 清风拂面

    谢谢分享学习

    0

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    2018-08-25 kafei

    学习了谢谢分享

    0

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    2018-08-25 深海的鱼

    学习学习学习

    0

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    2018-08-25 yjs木玉

    好好好好好好好好

    0

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