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[焦亡在牙周病发病机制中的研究进展]

[Advances in research of pyroptosis in the mechanism of periodontal disease].

作者信息

Yang M X, Ding P H, Kang S, Dong Y

机构信息

Department of Prosthodontics, The Second Affiliated Hospital of Zhejiang University School of Medicine, School of Stomatology, and Key Laboratory of Oral Biomedical Research of Zhejiang Province, Hangzhou 310009, China.

Department of Periodontology, Stomatology Hospital, School of Stomatology, Zhejiang University School of Medicine & Clinical Research Center for Oral Diseases of Zhejiang Province & Key Laboratory of Oral Biomedical Research of Zhejiang Province & Cancer Center of Zhejiang University, Hangzhou 310006, China.

出版信息

Zhonghua Kou Qiang Yi Xue Za Zhi. 2021 Sep 9;56(9):945-950. doi: 10.3760/cma.j.cn112144-20210506-00212.

Abstract

Pyroptosis is a pro-inflammatory form of programmed cell death that has been gradually recognized in recent years. It plays an important role in recognizing the invasion of exogenous pathogens and sensing endogenous danger signals. The initiation of pyroptosis depends on the activation of intracellular inflammasome and its downstream caspases, as well as the active fragment of the key protein Gasdermin. The invasion of periodontal pathogens induces an inflammatory response of the host, involving the activation of inflammasome and triggering pyroptosis as well. Meanwhile, it leads to the release of a large number of inflammatory cytokines such as interleukin (IL)-1β and IL-18 to amplify the inflammatory response and mediate periodontal tissue destruction eventually. This article reviews the research progress of the signaling pathways of pyroptosis, as well as its mechanism induced by periodontal pathogens and the mechanism of periodontal tissue damage in periodontitis in order to provide new targets and ideas for the prevention and treatment of periodontitis.

摘要

细胞焦亡是一种近年来逐渐被认识的程序性细胞死亡的促炎形式。它在识别外源性病原体的入侵和感知内源性危险信号方面发挥着重要作用。细胞焦亡的启动依赖于细胞内炎性小体及其下游半胱天冬酶的激活,以及关键蛋白Gasdermin的活性片段。牙周病原体的入侵诱导宿主的炎症反应,涉及炎性小体的激活并引发细胞焦亡。同时,它导致大量炎性细胞因子如白细胞介素(IL)-1β和IL-18的释放,以放大炎症反应并最终介导牙周组织破坏。本文综述了细胞焦亡信号通路的研究进展,以及牙周病原体诱导细胞焦亡的机制和牙周炎中牙周组织损伤的机制,以期为牙周炎的防治提供新的靶点和思路。

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