JCI：炎症疾病治疗新靶点--UCP2抑制剂有望治疗败血症

2015-01-12 MedSci MedSci原创

图示：UCP2-FASN调控脂质合成与NLRP3介导的caspase-1活化相关通路败血症是目前内科重症监护病房内患者死亡的最主要原因之一，而机体针对外源微生物产生的过度免疫应答反应是导致败血症发生的原因。细胞脂类代谢的水平及其变化与免疫应答密切相关。但是，体内脂肪酸的生成为何能够调节免疫应答，其内在机制尚未被明确阐释。炎症小体NLRP3能够作为前炎性细胞因子的caspase-1途径依赖的

图示：UCP2-FASN调控脂质合成与NLRP3介导的caspase-1活化相关通路

败血症是目前内科重症监护病房内患者死亡的最主要原因之一，而机体针对外源微生物产生的过度免疫应答反应是导致败血症发生的原因。细胞脂类代谢的水平及其变化与免疫应答密切相关。但是，体内脂肪酸的生成为何能够调节免疫应答，其内在机制尚未被明确阐释。炎症小体NLRP3能够作为前炎性细胞因子的caspase-1途径依赖的活化与分泌功能的重要平台。在本篇论文中，研究人员验证了线粒体解偶联蛋白（Mitochondrial Uncoupling Protein 2，UCP2）可以通过促进巨噬细胞中的脂质合成途径来调节NLRP3介导的caspase-1活化。该结果发表于2015年1月9日的Journal of Clinical Investigation杂志上。

研究人员在多种微生物引起的败血症的小鼠模型中发现，UCP2缺陷小鼠能够表现出更高的存活率。此外，在人类的败血症中，也可检测出UCP2表达升高。与以上结果一致的是，UCP2缺陷小鼠在接受LPS刺激后，表现出脂质合成功能受损、IL-1β与IL-18生成减少。在巨噬细胞中，UCP2缺陷能够抑制NLRP3介导的caspase-1的活化以及抑制脂质合成后导致的NLRP3的表达。在UCP2缺陷的巨噬细胞中，脂质合成的抑制是受上游的脂肪酸合成重要调节因子脂肪酸合成酶（fatty acid synthase，FASN）影响的。通过shRNA抑制FASN，以及使用化学抑制剂C75与浅蓝菌素能够抑制NLRP3介导的caspase-1的活化并抑制巨噬细胞内NLRP3与前IL-1β基因的表达。

因此研究人员得出结论，UCP2能够通过诱导巨噬细胞脂质合成通路调控NLRP3前炎症小体的表达。以上结果预示着UCP2有希望作为败血症等炎症相关疾病的潜在治疗靶点。

原始出处

Jong-Seok Moon1,2, Seonmin Lee3,4, Mi-Ae Park5 et.al.UCP2-induced fatty acid synthase promotes NLRP3 inflammasome activation during sepsis.JCI 2014

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2015-04-16 仁医06

#2抑制剂#

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2015-11-26 jklm09

#抑制剂#

38 0
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2015-04-06 qindq

#疾病治疗#

27 0
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2015-02-03 caobinglei8079

#JCI#

24 0
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2015-02-27 1249857fm32暂无昵称

#UCP2#

24 0
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2015-10-04 经常头晕

#炎症疾病#

24 0
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2015-01-14 lsndxfj

#新靶点#

21 0
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2015-01-14 12498f1em11(暂无昵称)

#治疗新靶点#

17 0

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JCI：炎症疾病治疗新靶点--UCP2抑制剂有望治疗败血症

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