坏死性凋亡分子机制及与牙周炎的相关性  

The molecular mechanism of necroptosis and its correlation with periodontitis

作　　者：孙欢欢 赵菲 陶然 刘冰[1] Sun Huanhuan;Zhao Fei;Tao Ran;Liu Bing(Hebei Medical University School and Hospital of Stomatology,Hebei Provincial Key Laboratory of Stomatology,Hebei Provincial Clinical Medical Research Center for Oral Diseases,Shijiazhuang 050017,Hebei Province,China)

机构地区：[1]河北医科大学口腔医学院·口腔医院,河北省口腔医学重点实验室,河北省口腔疾病临床医学研究中心,河北省石家庄市050017

出　　处：《中国组织工程研究》2025年第12期2569-2574,共6页Chinese Journal of Tissue Engineering Research

基　　金：河北省医学科学研究课题计划(20240512),项目名称:长链非编码RNA AC114812在牙周炎中的表达及调控机制研究,项目负责人:刘冰;河北省医学科学研究课题计划(20221454),项目名称:赤藓糖醇喷砂在慢性牙周炎患者维护期治疗中的效果研究,项目负责人:赵菲;河北省医学科学研究课题计划(20241077),项目名称:白藜芦醇纳米药物通过调控巨噬细胞极化治疗牙周炎的研究,项目负责人:陶然。

摘　　要：背景:近年来,随着细胞死亡研究的不断深入,坏死性凋亡逐渐成为学术界研究的热点和难点,其多种信号通路及蛋白在牙周炎的发生发展中起到不可忽视的作用,人们试图通过阻止细胞坏死性凋亡的发生,从而延缓牙周组织炎症的进程。目的:就坏死性凋亡的分子机制及其与牙周炎的相关性进行综述,期望为牙周炎的预防、诊断、治疗及预后提供新思路、新方向。方法:第一作者于2023年10月应用计算机检索PubMed、中国知网等数据库建库到2024年4月发表的相关文献,以“坏死性凋亡,细胞程序性死亡,牙周炎,牙周,免疫,炎症,受体相互作用蛋白激酶1,受体相互作用蛋白激酶3,混合系列蛋白激酶样结构域”为中文检索词;“necroptosis,programmed cell death,periodontitis,periodontal,immunity,inflammation,RIP1,RIP3,MLKL”为英文检索词,阅读每篇文献的文题、摘要、引言进行初步筛选,最终纳入56篇文献进行总结分析。结果与结论:①牙周炎的主要发病机制为牙周致病菌刺激机体,导致牙周微环境发生改变,打破原有免疫平衡并释放各种炎症因子,引发炎症反应造成牙周组织破坏,坏死性凋亡可以调控牙周组织免疫炎症反应,从而影响牙周炎的发生发展进程;②坏死性凋亡的发生与多种蛋白、信号通路及信号分子有关,已有动物实验证实了磷酸化混合系列蛋白激酶样结构域(pMLKL)的表达量与炎症程度有关,且在患有牙周炎小鼠的牙周组织中,RIP3和pMLKL高表达,通过阻断RIP3/MLKL通路,有利于减少牙周组织炎症、控制牙周炎的进展;③探究pMLKL是否可作为牙周炎的诊断指标,在牙周炎的预防、诊断及治疗上有很大价值。BACKGROUND:In recent years,with the deepening of cell death research,necroptosis has gradually become a hot and difficult topic in academic research.Its various signaling pathways and proteins play an important role in the occurrence and development of periodontitis.People try to delay the process of periodontal tissue inflammation by preventing the occurrence of necroptosis.OBJECTIVE:To provide a review on the molecular mechanism of necroptosis and its correlation with periodontitis in the hope of providing new ideas and directions for the prevention,diagnosis,treatment and evaluation of periodontitis.METHODS:The first author searched PubMed,CNKI,and other databases in October 2023 for relevant literature published up to April 2024 with the search terms of“necroptosis,programmed cell death,periodontitis,periodontal,immunity,inflammation,receptor interacting protein kinase 1,receptor interacting protein kinase 3,mixed lineage kinase domain-like”in Chinese and“necroptosis,programmed cell death,periodontitis,periodontal,immunity,inflammation,RIP1,RIP3,MLKL”in English,respectively.The titles and abstracts of each document were read for preliminary screening,and 56 documents were finally selected for generalization and analysis.RESULTS AND CONCLUSION:(1)The main pathogenesis of periodontitis is that periodontal pathogenic bacteria stimulate the organism,leading to changes in the periodontal microenvironment,breaking the original immune balance and releasing a variety of inflammatory factors,triggering an inflammatory response resulting in destruction of periodontal tissues.Necroptosis can modulate the immuno-inflammation in periodontal tissues,thus affecting the development of periodontitis.(2)The occurrence of necroptosis is related to a variety of proteins,signaling pathways,and signaling molecules.Animal experiments have confirmed that the expression of phosphorylated mixed lineage kinase domain-like protein(pMLKL)is related to the degree of inflammation,and RIP3 and pMLKL are highly expressed in the perio

关 键 词：坏死性凋亡 牙周炎 炎症 免疫 细胞程序性死亡 损伤相关分子模式 MLKL RIP3 

分 类 号：R459.9[医药卫生—治疗学] R318[医药卫生—临床医学] R781.4