NLRP3炎性体与代谢性疾病的研究进展
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南华大学,南华大学,南华大学,南华大学,南华大学,南华大学

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国家自然科学基金(81100213),湖南省研究生科研创新项目(2012SCX13)和国家级大学生创新创业训练计划(201210555018)资助项目


Research Advances of The NLRP3 Inflammasome and Metabolic Disease
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University of South China,University of South China,University of South China,University of South China,University of South China,University of South China

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This work was supported by grants from The National Natural Science Foundation of China (81100213), The Innovation Foundation for Postgraduate of Hunan Province (2012SCX13), The National College Students' Innovation and Entrepreneurship Training Program (201210555018)

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    摘要:

    代谢性疾病是由体内氨基酸、葡萄糖和脂质代谢紊乱引起的一类疾病,慢性炎症反应是其重要特征之一.Nod样受体蛋白3(Nod-like receptor protein 3,NLRP3)炎性体是位于细胞内的一种蛋白质复合体,主要功能为活化半胱氨酸天冬氨酸蛋白酶1(caspase-1)以间接调控白介素1β(IL-1β)、IL-18和IL-33等的成熟和分泌.NLRP3炎性体是炎性体相关研究的热点,多种内源性或外源性危险信号通过激活这一蛋白质复合体上调炎性因子的表达水平,从而促进多种代谢性疾病的发生发展.本文对NLRP3炎性体的结构、功能、调节以及在代谢性疾病中的作用做一综述,以期为代谢性疾病的防治提供新靶点.

    Abstract:

    Metabolic diseases are caused by amino acid, glucose and lipid metabolism disorder, chronic inflammation is one of its important characteristics. The Nod-like receptor protein 3 (NLRP3) inflammasome is a protein complexes located in cellular, the main function is to activate caspase -1, and then to indirectly regulate the mature and secretion of interleukin 1β (IL-1β), IL-18 and IL-33. The NLRP3 inflammasome is a hotspot in inflammasome associated studies, a variety of endogenous or exogenous danger signals up-regulated the expression of inflammatory cytokines through the activation of this protein complex, and promoted the occurrence and development of many metabolic diseases. Here we reviewed the structure, function and the regulation of the NLRP3 inflammasome, then discussed its role in metabolic diseases, in order to provide the new targets for the prevention and treatment of metabolic diseases.

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李金凤,谢笛,何平平,唐艳艳,涂玉林,尹凯. NLRP3炎性体与代谢性疾病的研究进展[J].生物化学与生物物理进展,2014,41(5):425-434

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历史
  • 收稿日期:2013-04-18
  • 最后修改日期:2013-08-26
  • 接受日期:2013-08-29
  • 在线发布日期: 2014-05-22
  • 出版日期: 2014-05-20