上海交通大学学报(医学版)

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去乙酰化酶在慢性炎症中的作用

莫兴兴,葛勤敏   

  1. 上海交通大学 医学院附属新华医院急诊科,上海 200092
  • 出版日期:2016-12-28 发布日期:2016-12-29
  • 通讯作者: 葛勤敏,电子信箱:geqinmin@126.com。
  • 作者简介:莫兴兴(1992—),女,硕士生;电子信箱:moxingxing6272@126.com。
  • 基金资助:

    上海市自然科学基金(14ZR1427000);国家临床重点专科

Role of sirtuins in chronic inflammatory diseases

MO Xing-xing, GE Qin-min   

  1. Department of Emergency, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200092, China
  • Online:2016-12-28 Published:2016-12-29
  • Supported by:

    Natural Science Foundation of Shanghai, 14ZR1427000;National Key Clinical Disciplines

摘要:

沉默信息调节因子(SIRTs)是一种烟酰胺腺嘌呤二核苷酸(NAD+)依赖的Ⅲ类组蛋白,其家族在调控氧化应激、炎症机制和衰老等方面发挥重要作用。在各种内外界刺激因素的作用下,机体产生大量促炎因子,抗炎、免疫机制被激活,但炎症因子若持续存在,最终会导致多器官的慢性炎症及组织的不断损伤。NAD+ 作为SIRTs发挥去乙酰化作用的辅助因子,可能通过调控组蛋白或NF-κB等转录因子的表达,减少促炎因子的产生;而SIRTs的敲除会进一步加重炎症反应侵害。因此,推测SIRTs可能是慢性炎症治疗的靶向分子。该文就SIRTs在各器官慢性炎症疾病发生中的作用以及涉及的信号分子作一综述,为慢性炎症疾病的治疗提供新的思路。

关键词: 沉默信息调节因子, 慢性炎症疾病, 生物代谢, 炎性介质

Abstract:

Silent information regulators (SIRTs) belong to classⅢhistone deacetylase family dependent on nicotinamide adenine dinucleotide (NAD+). SIRTs play important roles in regulating oxidative stress, inflammatory mechanisms, and senescence, etc. A large amount of proinflammatory cytokines will be produced under various internal and external stimuli and anti-inflammatory and immunologic mechanisms will be activated. But if inflammatory cytokines persistently exist in circulating system, they will eventually cause multi-organ chronic inflammation and tissue damage. As a deacetylation cofactor for SIRTs, NAD+ may reduce the production of inflammatory cytokines through regulating histones or transcription factors such as NF-κB. Knockout of SIRTs will aggravate inflammatory invasion. So SIRTs may be a potential target for the treatment of chronic inflammatory diseases. This article reviews the role of SIRTs in the occurrence of different chronic inflammatory diseases and related signaling molecules with the aim to provide novel ideas for the treatment of chronic inflammatory diseases.

Key words: silent information regulators, chronic inflammatory diseases, biological metabolism, inflammatory mediators